rdf:type |
|
lifeskim:mentions |
umls-concept:C0004359,
umls-concept:C0021368,
umls-concept:C0039194,
umls-concept:C0085358,
umls-concept:C0205224,
umls-concept:C0443146,
umls-concept:C0444498,
umls-concept:C0524637,
umls-concept:C1052868,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1706438,
umls-concept:C2698600
|
pubmed:issue |
20
|
pubmed:dateCreated |
2010-5-20
|
pubmed:abstractText |
A current paradigm states that non-antigen-specific inflammatory cues attract noncognate, bystander T cell specificities to sites of infection and autoimmune inflammation. Here we show that cues emanating from a tissue undergoing spontaneous autoimmune inflammation cannot recruit naive or activated bystander T cell specificities in the absence of local expression of cognate antigen. We monitored the recruitment of CD8(+) T cells specific for the prevalent diabetogenic epitope islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP)(206-214) in gene-targeted nonobese diabetic (NOD) mice expressing a T cell "invisible" IGRP(206-214) sequence. These mice developed islet inflammation and diabetes with normal incidence and kinetics, but their inflammatory lesions could recruit neither naive (endogenous or exogenous) nor ex vivo-activated IGRP(206-214)-reactive CD8(+) T cells. Conversely, IGRP(206-214)-reactive, but not nonautoreactive CD8(+) T cells rapidly homed to and accumulated in the inflamed islets of wild-type NOD mice. Our results indicate that CD8(+) T cell recruitment to a site of autoimmune inflammation results from an active process that is strictly dependent on local display of cognate pMHC and suggest that CD8(+) T cells contained in extralymphoid autoimmune lesions are largely autoreactive.
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pubmed:grant |
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-10036638,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-10430939,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-10470079,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-10963600,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-11018170,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-11441068,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-12421921,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-12531877,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-12615905,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-12750472,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-12811844,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-12815107,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-14617043,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-14662897,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-14702111,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-14768060,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-15070692,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-15761850,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-15795256,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-16148094,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-16308575,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-16580261,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-16920977,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-17880383,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-18782577,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-19111164,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-19818656,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-7682590,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-7860730,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-8386207,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-8746560,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-8906855,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-9064356,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-9362527,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-9790722,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20439719-9864948
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1091-6490
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pubmed:author |
|
pubmed:issnType |
Electronic
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pubmed:day |
18
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pubmed:volume |
107
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
9317-22
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pubmed:dateRevised |
2010-9-28
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pubmed:meshHeading |
pubmed-meshheading:20439719-Adoptive Transfer,
pubmed-meshheading:20439719-Analysis of Variance,
pubmed-meshheading:20439719-Animals,
pubmed-meshheading:20439719-Autoantigens,
pubmed-meshheading:20439719-Autoimmunity,
pubmed-meshheading:20439719-CD8-Positive T-Lymphocytes,
pubmed-meshheading:20439719-Diabetes Mellitus, Type 1,
pubmed-meshheading:20439719-Epitopes, T-Lymphocyte,
pubmed-meshheading:20439719-Flow Cytometry,
pubmed-meshheading:20439719-Glucose-6-Phosphatase,
pubmed-meshheading:20439719-Islets of Langerhans,
pubmed-meshheading:20439719-Mice,
pubmed-meshheading:20439719-Mice, Inbred NOD,
pubmed-meshheading:20439719-Mice, Transgenic,
pubmed-meshheading:20439719-Microscopy, Confocal,
pubmed-meshheading:20439719-Proteins
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pubmed:year |
2010
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pubmed:articleTitle |
In situ recognition of autoantigen as an essential gatekeeper in autoimmune CD8+ T cell inflammation.
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pubmed:affiliation |
Julia McFarlane Diabetes Research Centre and Department of Microbiology and Infectious Diseases,, University of Calgary, Calgary, AB, Canada T2N 4N1.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|