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Antigen‐Induced Death Of Mature T Lymphocytes: Analysis By Flow Cytometry

D. Kabelitz, H. Oberg, T. Pohl, K. Pechhold
Published 1994 · Biology, Medicine

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Signalling via the CD3/T-cell receptor (TCR) complex or via alternative pathways (e.g., CD2) induces the activation of resting T cells; "activation" is characterized by the rapid increase of intracellular Cd}'^ levels, induction of cytokine genes, and cellular proliferation (Meuer et al. 1984a, 1984b). The process of CD3/TCR signalling is strongly modulated by additional cell surface antigens such as the p56'''^ associated coreceptors CD4/CD8 and the tyrosine phosphatase-associated CD45 molecule (Janeway 1992). Studies on the intrathymic T-cell development revealed that the same signals which stimulate resting T cells also trigger programmed cell death (apoptosis) in immature thymocytes as well as in transformed T cells (hybridomas or leukemic T cells) (Ashwell et al. 1987, Odaka etal. 1989, Smith et al. 1989, Tadakuma et al. 1990, Takahashi et al. 1989, Ucker et al. 1989). Anti gen-induced apoptosis of immature thymocytes is thought to be the major mechanism for negative selection of the developing T-cell receptor repertoire (MacDonald 1990, Jenkinson et al. 1989. von Boehmer 1992). More recently, it became clear that activationinduced cell death (AICD) is not restricted to immature thymocytes and transformed T lymphocytes but can be similarly induced in mature peripheral T cells. While the initial data showed that non-specific stimuli such as mitogenic lectins (e.g., PHA) or anti-CD3/TCR monoclonal antibodies (mAb) triggered apoptosis in activated mature T cells (Janssen et al. 1991, Liu & Janeway 1990. Russell ct al. 1991, Ucker et al. 1992, Wesselborg & Kabelitz 1993), accumulating evidence suggests that this is also true for superantigens and even conventional antigens (D'Adamio et al. 1993, Kabelitz & Wesselborg 1992, Kawabe & Ochi 1991, MacDonald et al.
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