Participation of target Fas protein in apoptosis pathway induced by CD4+ Th1 and CD8+ cytotoxic T cells
摘要：
The results presented here provide evidence that the presence of Fas protein in target cells is essential to permit cytotoxicity (resulting in apoptosis) mediated by cloned CD4+Th1 cells. Using mitogen-activated B cells as targets, antigen-dependent lysis by CD4+Th1 effectors was observed with MRL/MpJ+ but not with MRL/MpJ-lpr targets. The congenic MRL/MpJ-lpr strain is defective in Fas expression. Target cells from various lymphoid tissues of C3H.MRL-lpr mice were also resistant to the lectin-dependent cytotoxicity of Th1 effectors, whereas C3H/HeJ targets were sensitive. Moreover, a rapid DNA fragmentation prior to51Cr release was induced only in C3H/HeJ targets. Thus, cytotoxicity induced by Th1 effectors correlates with target Fas expression. In contrast to Th1 effectors, CD8+cytotoxic T lymphocytes (CTLs) killed C3H.MRL-lpr targets. When cytotoxicity was assayed in the presence of EGTA and MgCl2, which chelates extracellular Ca2+[(Ca2+)ext], only C3H.MRL-lpr targets became resistant to CD8+CTLs. This (Ca2+)ext-independent cytotoxicity of both Th1 and CD8+effectors could be inhibited with unlabeled C3H/HeJ thymocytes or with a transfectoma carrying a murine Fas-human μ gene construct. In comparison, C3H.MRL-lpr thymocytes and the nontransfected parental cell line were poor inhibitors. Our study demonstrates that CD4+Th1 cells and CD8+CTLs differ in their (Ca2+)ext-dependent cytotoxicity but share a (Ca2+)ext-independent cytotoxicity that requires participation of Fas molecules for cytotoxic signal transduction leading to target apoptosis.
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DOI：
10.1073/pnas.91.10.4185
被引量：
年份：
1994
Wiley
万方医学
Semantic Scholar
掌桥科研
dx.doi.org
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