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. 2009 Aug;9(8):1784-95.
doi: 10.1111/j.1600-6143.2009.02723.x. Epub 2009 Jun 26.

"V体育官网入口" Primed CD8(+) T-cell responses to allogeneic endothelial cells are controlled by local complement activation

H Raedler  1 , M Yang, P N Lalli, M E Medof, P S Heeger
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Primed CD8(+) T-cell responses to allogeneic endothelial cells are controlled by local complement activation (V体育安卓版)

H Raedler et al. Am J Transplant. 2009 Aug.
Free article

Abstract

CD8 T cells primed by transplantation recognize allogeneic class I MHC molecules expressed on graft vascular endothelium and contribute to allograft injury. We previously showed that immune cell-derived complement activation fragments are integral to T cell activation/expansion. Herein we tested the impact of local complement production/activation on T cell/endothelial cell (EC) interactions. We found that proinflammatory cytokines upregulated alternative pathway complement production by ECs, yielding C5a. We further found that ECs deficient in the cell surface C3/C5 convertase regulator decay accelerating factor (DAF, CD55) induced greater CD8 T-cell proliferation and more IFNgamma(+) and perforin(+) effector cells than wild-type (WT) ECs. Allogeneic C3(-/-) EC induced little or no CD8 responses. Abrogation of responses following C5a receptor (C5aR) blockade, or augmentation following addition of recombinant C5a demonstrated that the effects were mediated through T-cell-expressed-C5aR interactions. Analyses of in vivo CD8 cell responses to transplanted heart grafts deficient in EC DAF showed similar augmentation. The findings reveal that EC-derived complement triggers secondary CD8 T-cell differentiation and expansion and argue that targeting complement and/or C5aR could limit T-cell-mediated graft injury VSports手机版. .

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