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CD4 T cells kill melanoma cells by mechanisms that are independent of Fas (CD95)
Author(s) -
Thomas Wayne D.,
Hersey Peter
Publication year - 1998
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19980130)75:3<384::aid-ijc10>3.0.co;2-9
Subject(s) - fas ligand , cytotoxic t cell , melanoma , fas receptor , apoptosis , cancer research , immunology , biology , adoptive cell transfer , major histocompatibility complex , t cell , immune system , programmed cell death , in vitro , biochemistry
Previous studies have shown that CD4 T cells are associated with regression in primary melanoma and rejection of tumors in adoptive transfer models. The mechanism by which they mediate their anti‐tumor effects remains unclear, and some studies have suggested that Fas ligand (FasL)/Fas interactions were involved. In the present study, we have examined the cytotoxic mechanism involved in CD4 T‐cell killing of melanoma cells and, in particular, the role of FasL/Fas interactions in this killing. We show that the CD4 T cells in 4 clones of T cells induced apoptosis in autologous melanoma cells by MHC‐restricted mechanisms but lysed an allogeneic melanoma cell by a non‐apoptotic mechanism. Melanoma cells expressed both Fas and FasL, but killing of melanoma cells did not involve Fas/FasL interactions. This was shown by a lack of correlation between Fas expression and susceptibility to lysis and by failure of a monoclonal antibody to Fas to block killing by the CD4 T cells, though the latter expressed FasL. Recombinant FasL did not induce killing of melanoma cells. Int. J. Cancer 75:384–390, 1998. © 1998 Wiley‐Liss, Inc.