| First Author | Edgerton C | Year | 2009 |
| Journal | Clin Immunol | Volume | 130 |
| Issue | 3 | Pages | 313-21 |
| PubMed ID | 19058762 | Mgi Jnum | J:145181 |
| Mgi Id | MGI:3833792 | Doi | 10.1016/j.clim.2008.09.019 |
| Citation | Edgerton C, et al. (2009) IL-17 producing CD4+ T cells mediate accelerated ischemia/reperfusion-induced injury in autoimmunity-prone mice. Clin Immunol 130(3):313-21 |
| abstractText | 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/lpr 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 role in intestinal I/R damage by virtue of producing the pro-inflammatory cytokine IL-17. |
