Author/Authors :
Edgerton، نويسنده , , Colin and Crispيn، نويسنده , , José C. and Moratz، نويسنده , , Chantal M. and Bettelli، نويسنده , , Estelle and Oukka، نويسنده , , Mohamed and Simovic، نويسنده , , Milomir and Zacharia، نويسنده , , Athina and Egan، نويسنده , , Ryan and Chen، نويسنده , , Jie and Dalle Lucca، نويسنده , , Jurandir J. and Juang، نويسنده , , Yuang-Taung and Tsokos، نويسنده , , George C.، نويسنده ,
Abstract :
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.
Keywords :
systemic lupus erythematosus , T cell , Autoimmunity , IL-17 , inflammation , MRL/lpr mice , ischemia reperfusion , IL-23 , p19?/? mice
