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<p class=MsoNormal><span style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:
"Times New Roman";color:#333333;background:white'>The role of the unfolded
protein response (UPR) and endoplasmic reticulum (ER) stress in homeostasis of
the immune system is incompletely understood. Here we found that dendritic
cells (DCs) constitutively activated the UPR sensor IRE-1</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and its target, the transcription factor
XBP-1, in the absence of ER stress. Loss of XBP-1 in CD11c</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;cells led to defects in phenotype, ER homeostasis and
antigen presentation by CD8</span><span style='font-size:11.0pt;font-family:
Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:"Times New Roman";
color:#333333;background:white'>&#945;</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;conventional
DCs, yet the closely related CD11b</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;DCs
were unaffected. Whereas the dysregulated ER in XBP-1-deficient DCs resulted
from loss of XBP-1 transcriptional activity, the phenotypic and functional
defects resulted from regulated IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>-dependent degradation (RIDD) of mRNAs,
including those encoding CD18 integrins and components of the major
histocompatibility complex (MHC) class I machinery. Thus, a precisely regulated
feedback circuit involving IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and XBP-1 controls the homeostasis of CD8</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;conventional DCs.</span><span style='font-size:10.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman"'><o:p></o:p></span></p>

<p class=MsoNormal><o:p>&nbsp;</o:p></p>

<p class=MsoNormal><span style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:
"Times New Roman";color:#333333;background:white'>The role of the unfolded
protein response (UPR) and endoplasmic reticulum (ER) stress in homeostasis of
the immune system is incompletely understood. Here we found that dendritic
cells (DCs) constitutively activated the UPR sensor IRE-1</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and its target, the transcription factor
XBP-1, in the absence of ER stress. Loss of XBP-1 in CD11c</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;cells led to defects in phenotype, ER homeostasis and
antigen presentation by CD8</span><span style='font-size:11.0pt;font-family:
Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:"Times New Roman";
color:#333333;background:white'>&#945;</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;conventional
DCs, yet the closely related CD11b</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;DCs
were unaffected. Whereas the dysregulated ER in XBP-1-deficient DCs resulted
from loss of XBP-1 transcriptional activity, the phenotypic and functional
defects resulted from regulated IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>-dependent degradation (RIDD) of mRNAs,
including those encoding CD18 integrins and components of the major
histocompatibility complex (MHC) class I machinery. Thus, a precisely regulated
feedback circuit involving IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and XBP-1 controls the homeostasis of CD8</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;conventional DCs.</span><span style='font-size:10.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman"'><o:p></o:p></span></p>

<p class=MsoNormal><span style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:
"Times New Roman";color:#333333;background:white'>The role of the unfolded
protein response (UPR) and endoplasmic reticulum (ER) stress in homeostasis of
the immune system is incompletely understood. Here we found that dendritic
cells (DCs) constitutively activated the UPR sensor IRE-1</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and its target, the transcription factor
XBP-1, in the absence of ER stress. Loss of XBP-1 in CD11c</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;cells led to defects in phenotype, ER homeostasis and
antigen presentation by CD8</span><span style='font-size:11.0pt;font-family:
Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:"Times New Roman";
color:#333333;background:white'>&#945;</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;conventional
DCs, yet the closely related CD11b</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;DCs
were unaffected. Whereas the dysregulated ER in XBP-1-deficient DCs resulted
from loss of XBP-1 transcriptional activity, the phenotypic and functional
defects resulted from regulated IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>-dependent degradation (RIDD) of mRNAs,
including those encoding CD18 integrins and components of the major
histocompatibility complex (MHC) class I machinery. Thus, a precisely regulated
feedback circuit involving IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and XBP-1 controls the homeostasis of CD8</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;conventional DCs.</span><span style='font-size:10.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman"'><o:p></o:p></span></p>

<p class=MsoNormal><o:p>&nbsp;</o:p></p>

<p class=MsoNormal><span style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:
"Times New Roman";color:#333333;background:white'>The role of the unfolded
protein response (UPR) and endoplasmic reticulum (ER) stress in homeostasis of
the immune system is incompletely understood. Here we found that dendritic
cells (DCs) constitutively activated the UPR sensor IRE-1</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and its target, the transcription factor
XBP-1, in the absence of ER stress. Loss of XBP-1 in CD11c</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;cells led to defects in phenotype, ER homeostasis and
antigen presentation by CD8</span><span style='font-size:11.0pt;font-family:
Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:"Times New Roman";
color:#333333;background:white'>&#945;</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;conventional
DCs, yet the closely related CD11b</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;DCs
were unaffected. Whereas the dysregulated ER in XBP-1-deficient DCs resulted
from loss of XBP-1 transcriptional activity, the phenotypic and functional
defects resulted from regulated IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>-dependent degradation (RIDD) of mRNAs,
including those encoding CD18 integrins and components of the major
histocompatibility complex (MHC) class I machinery. Thus, a precisely regulated
feedback circuit involving IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and XBP-1 controls the homeostasis of CD8</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;conventional DCs.</span><span style='font-size:10.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman"'><o:p></o:p></span></p>

<p class=MsoNormal><o:p>&nbsp;</o:p></p>

<p class=MsoNormal><span style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:
"Times New Roman";color:#333333;background:white'>The role of the unfolded
protein response (UPR) and endoplasmic reticulum (ER) stress in homeostasis of
the immune system is incompletely understood. Here we found that dendritic
cells (DCs) constitutively activated the UPR sensor IRE-1</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and its target, the transcription factor
XBP-1, in the absence of ER stress. Loss of XBP-1 in CD11c</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;cells led to defects in phenotype, ER homeostasis and
antigen presentation by CD8</span><span style='font-size:11.0pt;font-family:
Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:"Times New Roman";
color:#333333;background:white'>&#945;</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;conventional
DCs, yet the closely related CD11b</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;DCs
were unaffected. Whereas the dysregulated ER in XBP-1-deficient DCs resulted
from loss of XBP-1 transcriptional activity, the phenotypic and functional
defects resulted from regulated IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>-dependent degradation (RIDD) of mRNAs,
including those encoding CD18 integrins and components of the major
histocompatibility complex (MHC) class I machinery. Thus, a precisely regulated
feedback circuit involving IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and XBP-1 controls the homeostasis of CD8</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;conventional DCs.</span><span style='font-size:10.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman"'><o:p></o:p></span></p>

<p class=MsoNormal><o:p>&nbsp;</o:p></p>

<p class=MsoNormal><span style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:
"Times New Roman";color:#333333;background:white'>The role of the unfolded
protein response (UPR) and endoplasmic reticulum (ER) stress in homeostasis of
the immune system is incompletely understood. Here we found that dendritic
cells (DCs) constitutively activated the UPR sensor IRE-1</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and its target, the transcription factor
XBP-1, in the absence of ER stress. Loss of XBP-1 in CD11c</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;cells led to defects in phenotype, ER homeostasis and
antigen presentation by CD8</span><span style='font-size:11.0pt;font-family:
Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:"Times New Roman";
color:#333333;background:white'>&#945;</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;conventional
DCs, yet the closely related CD11b</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;DCs
were unaffected. Whereas the dysregulated ER in XBP-1-deficient DCs resulted
from loss of XBP-1 transcriptional activity, the phenotypic and functional
defects resulted from regulated IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>-dependent degradation (RIDD) of mRNAs,
including those encoding CD18 integrins and components of the major
histocompatibility complex (MHC) class I machinery. Thus, a precisely regulated
feedback circuit involving IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and XBP-1 controls the homeostasis of CD8</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;conventional DCs.</span><span style='font-size:10.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman"'><o:p></o:p></span></p>

<p class=MsoNormal><o:p>&nbsp;</o:p></p>

<p class=MsoNormal><span style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:
"Times New Roman";color:#333333;background:white'>The role of the unfolded
protein response (UPR) and endoplasmic reticulum (ER) stress in homeostasis of
the immune system is incompletely understood. Here we found that dendritic
cells (DCs) constitutively activated the UPR sensor IRE-1</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and its target, the transcription factor
XBP-1, in the absence of ER stress. Loss of XBP-1 in CD11c</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;cells led to defects in phenotype, ER homeostasis and
antigen presentation by CD8</span><span style='font-size:11.0pt;font-family:
Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:"Times New Roman";
color:#333333;background:white'>&#945;</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;conventional
DCs, yet the closely related CD11b</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;DCs
were unaffected. Whereas the dysregulated ER in XBP-1-deficient DCs resulted
from loss of XBP-1 transcriptional activity, the phenotypic and functional
defects resulted from regulated IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>-dependent degradation (RIDD) of mRNAs,
including those encoding CD18 integrins and components of the major
histocompatibility complex (MHC) class I machinery. Thus, a precisely regulated
feedback circuit involving IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and XBP-1 controls the homeostasis of CD8</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;conventional DCs.</span><span style='font-size:10.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman"'><o:p></o:p></span></p>

<p class=MsoNormal><o:p>&nbsp;</o:p></p>

<p class=MsoNormal><span style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:
"Times New Roman";color:#333333;background:white'>The role of the unfolded
protein response (UPR) and endoplasmic reticulum (ER) stress in homeostasis of
the immune system is incompletely understood. Here we found that dendritic
cells (DCs) constitutively activated the UPR sensor IRE-1</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and its target, the transcription factor
XBP-1, in the absence of ER stress. Loss of XBP-1 in CD11c</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;cells led to defects in phenotype, ER homeostasis and
antigen presentation by CD8</span><span style='font-size:11.0pt;font-family:
Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:"Times New Roman";
color:#333333;background:white'>&#945;</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;conventional
DCs, yet the closely related CD11b</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;DCs
were unaffected. Whereas the dysregulated ER in XBP-1-deficient DCs resulted
from loss of XBP-1 transcriptional activity, the phenotypic and functional
defects resulted from regulated IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>-dependent degradation (RIDD) of mRNAs,
including those encoding CD18 integrins and components of the major
histocompatibility complex (MHC) class I machinery. Thus, a precisely regulated
feedback circuit involving IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and XBP-1 controls the homeostasis of CD8</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;conventional DCs.</span><span style='font-size:10.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman"'><o:p></o:p></span></p>

<p class=MsoNormal><span style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:
"Times New Roman";color:#333333;background:white'>The role of the unfolded
protein response (UPR) and endoplasmic reticulum (ER) stress in homeostasis of
the immune system is incompletely understood. Here we found that dendritic
cells (DCs) constitutively activated the UPR sensor IRE-1</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and its target, the transcription factor
XBP-1, in the absence of ER stress. Loss of XBP-1 in CD11c</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;cells led to defects in phenotype, ER homeostasis and
antigen presentation by CD8</span><span style='font-size:11.0pt;font-family:
Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:"Times New Roman";
color:#333333;background:white'>&#945;</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;conventional
DCs, yet the closely related CD11b</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;DCs
were unaffected. Whereas the dysregulated ER in XBP-1-deficient DCs resulted
from loss of XBP-1 transcriptional activity, the phenotypic and functional
defects resulted from regulated IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>-dependent degradation (RIDD) of mRNAs,
including those encoding CD18 integrins and components of the major
histocompatibility complex (MHC) class I machinery. Thus, a precisely regulated
feedback circuit involving IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and XBP-1 controls the homeostasis of CD8</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;conventional DCs.</span><span style='font-size:10.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman"'><o:p></o:p></span></p>

<p class=MsoNormal><o:p>&nbsp;</o:p></p>

<p class=MsoNormal><span style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:
"Times New Roman";color:#333333;background:white'>The role of the unfolded
protein response (UPR) and endoplasmic reticulum (ER) stress in homeostasis of
the immune system is incompletely understood. Here we found that dendritic
cells (DCs) constitutively activated the UPR sensor IRE-1</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and its target, the transcription factor
XBP-1, in the absence of ER stress. Loss of XBP-1 in CD11c</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;cells led to defects in phenotype, ER homeostasis and
antigen presentation by CD8</span><span style='font-size:11.0pt;font-family:
Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:"Times New Roman";
color:#333333;background:white'>&#945;</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;conventional
DCs, yet the closely related CD11b</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;DCs
were unaffected. Whereas the dysregulated ER in XBP-1-deficient DCs resulted
from loss of XBP-1 transcriptional activity, the phenotypic and functional
defects resulted from regulated IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>-dependent degradation (RIDD) of mRNAs,
including those encoding CD18 integrins and components of the major
histocompatibility complex (MHC) class I machinery. Thus, a precisely regulated
feedback circuit involving IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and XBP-1 controls the homeostasis of CD8</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;conventional DCs.</span><span style='font-size:10.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman"'><o:p></o:p></span></p>

<p class=MsoNormal><o:p>&nbsp;</o:p></p>

<p class=MsoNormal><span style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:
"Times New Roman";color:#333333;background:white'>The role of the unfolded
protein response (UPR) and endoplasmic reticulum (ER) stress in homeostasis of
the immune system is incompletely understood. Here we found that dendritic
cells (DCs) constitutively activated the UPR sensor IRE-1</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and its target, the transcription factor
XBP-1, in the absence of ER stress. Loss of XBP-1 in CD11c</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;cells led to defects in phenotype, ER homeostasis and
antigen presentation by CD8</span><span style='font-size:11.0pt;font-family:
Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:"Times New Roman";
color:#333333;background:white'>&#945;</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;conventional
DCs, yet the closely related CD11b</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;DCs
were unaffected. Whereas the dysregulated ER in XBP-1-deficient DCs resulted
from loss of XBP-1 transcriptional activity, the phenotypic and functional
defects resulted from regulated IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>-dependent degradation (RIDD) of mRNAs,
including those encoding CD18 integrins and components of the major
histocompatibility complex (MHC) class I machinery. Thus, a precisely regulated
feedback circuit involving IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and XBP-1 controls the homeostasis of CD8</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;conventional DCs.</span><span style='font-size:10.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman"'><o:p></o:p></span></p>

<p class=MsoNormal><o:p>&nbsp;</o:p></p>

<p class=MsoNormal><span style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:
"Times New Roman";color:#333333;background:white'>The role of the unfolded
protein response (UPR) and endoplasmic reticulum (ER) stress in homeostasis of
the immune system is incompletely understood. Here we found that dendritic
cells (DCs) constitutively activated the UPR sensor IRE-1</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and its target, the transcription factor
XBP-1, in the absence of ER stress. Loss of XBP-1 in CD11c</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;cells led to defects in phenotype, ER homeostasis and
antigen presentation by CD8</span><span style='font-size:11.0pt;font-family:
Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:"Times New Roman";
color:#333333;background:white'>&#945;</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;conventional
DCs, yet the closely related CD11b</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;DCs
were unaffected. Whereas the dysregulated ER in XBP-1-deficient DCs resulted
from loss of XBP-1 transcriptional activity, the phenotypic and functional
defects resulted from regulated IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>-dependent degradation (RIDD) of mRNAs,
including those encoding CD18 integrins and components of the major
histocompatibility complex (MHC) class I machinery. Thus, a precisely regulated
feedback circuit involving IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and XBP-1 controls the homeostasis of CD8</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;conventional DCs.</span><span style='font-size:10.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman"'><o:p></o:p></span></p>

<p class=MsoNormal><o:p>&nbsp;</o:p></p>

<p class=MsoNormal><span style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:
"Times New Roman";color:#333333;background:white'>The role of the unfolded
protein response (UPR) and endoplasmic reticulum (ER) stress in homeostasis of
the immune system is incompletely understood. Here we found that dendritic
cells (DCs) constitutively activated the UPR sensor IRE-1</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and its target, the transcription factor
XBP-1, in the absence of ER stress. Loss of XBP-1 in CD11c</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;cells led to defects in phenotype, ER homeostasis and
antigen presentation by CD8</span><span style='font-size:11.0pt;font-family:
Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:"Times New Roman";
color:#333333;background:white'>&#945;</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;conventional
DCs, yet the closely related CD11b</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;DCs
were unaffected. Whereas the dysregulated ER in XBP-1-deficient DCs resulted
from loss of XBP-1 transcriptional activity, the phenotypic and functional
defects resulted from regulated IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>-dependent degradation (RIDD) of mRNAs,
including those encoding CD18 integrins and components of the major
histocompatibility complex (MHC) class I machinery. Thus, a precisely regulated
feedback circuit involving IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and XBP-1 controls the homeostasis of CD8</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;conventional DCs.</span><span style='font-size:10.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman"'><o:p></o:p></span></p>

<p class=MsoNormal><o:p>&nbsp;</o:p></p>

<p class=MsoNormal><span style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:
"Times New Roman";color:#333333;background:white'>The role of the unfolded
protein response (UPR) and endoplasmic reticulum (ER) stress in homeostasis of
the immune system is incompletely understood. Here we found that dendritic
cells (DCs) constitutively activated the UPR sensor IRE-1</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and its target, the transcription factor
XBP-1, in the absence of ER stress. Loss of XBP-1 in CD11c</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;cells led to defects in phenotype, ER homeostasis and
antigen presentation by CD8</span><span style='font-size:11.0pt;font-family:
Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:"Times New Roman";
color:#333333;background:white'>&#945;</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;conventional
DCs, yet the closely related CD11b</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;DCs
were unaffected. Whereas the dysregulated ER in XBP-1-deficient DCs resulted
from loss of XBP-1 transcriptional activity, the phenotypic and functional
defects resulted from regulated IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>-dependent degradation (RIDD) of mRNAs,
including those encoding CD18 integrins and components of the major
histocompatibility complex (MHC) class I machinery. Thus, a precisely regulated
feedback circuit involving IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and XBP-1 controls the homeostasis of CD8</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;conventional DCs.</span><span style='font-size:10.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman"'><o:p></o:p></span></p>

<p class=MsoNormal><o:p>&nbsp;</o:p></p>

<p class=MsoNormal><span style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:
"Times New Roman";color:#333333;background:white'>The role of the unfolded
protein response (UPR) and endoplasmic reticulum (ER) stress in homeostasis of
the immune system is incompletely understood. Here we found that dendritic
cells (DCs) constitutively activated the UPR sensor IRE-1</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and its target, the transcription factor
XBP-1, in the absence of ER stress. Loss of XBP-1 in CD11c</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;cells led to defects in phenotype, ER homeostasis and
antigen presentation by CD8</span><span style='font-size:11.0pt;font-family:
Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:"Times New Roman";
color:#333333;background:white'>&#945;</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;conventional
DCs, yet the closely related CD11b</span><sup><span style='font-size:9.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>+</span></sup><span style='font-size:11.0pt;font-family:Arial;
mso-fareast-font-family:"Times New Roman";color:#333333;background:white'>&nbsp;DCs
were unaffected. Whereas the dysregulated ER in XBP-1-deficient DCs resulted
from loss of XBP-1 transcriptional activity, the phenotypic and functional
defects resulted from regulated IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>-dependent degradation (RIDD) of mRNAs,
including those encoding CD18 integrins and components of the major
histocompatibility complex (MHC) class I machinery. Thus, a precisely regulated
feedback circuit involving IRE-1</span><span style='font-size:11.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman";color:#333333;background:white'>&#945;</span><span
style='font-size:11.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>&nbsp;and XBP-1 controls the homeostasis of CD8</span><span
style='font-size:11.0pt;font-family:Times;mso-fareast-font-family:"Times New Roman";
mso-bidi-font-family:"Times New Roman";color:#333333;background:white'>&#945;</span><sup><span
style='font-size:9.0pt;font-family:Arial;mso-fareast-font-family:"Times New Roman";
color:#333333;background:white'>+</span></sup><span style='font-size:11.0pt;
font-family:Arial;mso-fareast-font-family:"Times New Roman";color:#333333;
background:white'>&nbsp;conventional DCs.</span><span style='font-size:10.0pt;
font-family:Times;mso-fareast-font-family:"Times New Roman";mso-bidi-font-family:
"Times New Roman"'><o:p></o:p></span></p>

<p class=MsoNormal><o:p>&nbsp;</o:p></p>

<p class=MsoNormal><o:p>&nbsp;</o:p></p>

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