CD3+ CD8+ NKG2D+ T Lymphocytes Induce Apoptosis and Necroptosis in HLA-Negative Cells via FasL-Fas Interaction.

摘要: An important problem in cellular immunology is to identify new populations of cytotoxic lymphocytes capable killing tumor cells that have lost classical components MHC-machinery and understand mechanisms the death these cells. We previously found CD4+ CD25+ appear lymphokine-activated killer (LAK) cell culture, which carry Tag7 (PGRP-S) FasL proteins on their surface can kill Hsp70- Fas-expressing HLA-negative In this work, we continued study cells, focusing time CD8+ lymphocytes. show after a antigen contact IL-2 activated acquire ability lyse bearing antigen. However, activation absence causes appearance population NKG2D+ lymphocytes, are able cancer classic mechanism presentation. These recognize noncanonical MicA K562 but them via FasL-Fas interaction, as do T presented lymphocyte trigger both apoptosis necroptosis. Unlike case TNFR1, another receptor, no switching alternative processes has been observed upon induction Fas-dependent death. It may well be apoptotic necroptotic signals transduced separately latter case, with FasL+ induce necroptosis allowing escape apoptosis. J. Cell. Biochem. 118: 3359-3366, 2017. © 2017 Wiley Periodicals, Inc.