Journal
CLINICAL IMMUNOLOGY
Volume 130, Issue 3, Pages 313-321Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.clim.2008.09.019
Keywords
Autoimmunity; IL-17; IL-23; Inflammation; Ischemia reperfusion; MRL/lpr mice; p19(-/-) mice; Systemic lupus; erythematosus; T cell
Categories
Funding
- National Institutes of Health [R01 A142269]
- Medical Research Command [W81XWH-07-1-0286, W81XWH-06-1-0486]
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Elements of the innate and adaptive immune response have been implicated in the development of tissue damage after ischemic reperfusion (I/R). Here we demonstrate that T cells infiltrate the intestine of C57BL/6 mice subjected to intestinal I/R during the first hour of reperfusion. The intensity of the T cell infiltration was higher in B6.MRL/lpr mice subjected to intestinal I/R and reflected more severe tissue damage than that observed in control mice. Depletion of T cells limited I/R damage in B6.MRL/lpr mice, whereas repletion of B6.MRL/Ipr lymph node-derived T cells into the I/R-resistant Rag-1(-/-) mouse reconstituted tissue injury. The tissue-infiltrating T cells were found to produce IL-17. Finally, IL-23 deficient mice, which are known not to produce IL-17, displayed significantly less intestinal damage when subjected to I/R. Our data assign T cells a major rote in intestinal I/R damage by virtue of producing the proinflammatory cytokine IL-17. (C) 2008 Elsevier Inc. All rights reserved.
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