Figure 1.
Figure 1. Physiologic regulation of immune responses by Fas/FasL-induced apoptosis. (A) Activation of T cells by the engagement of T-cell receptors (TCR) with the peptide/major histocompatibility complex (MHC) bimolecular complex in conjunction with the transduction of secondary signals (not shown) leads to the up-regulation of both Fas and FasL expression. (B) Upon repeated antigenic stimulation, T cells become sensitive to Fas/FasL-mediated apoptosis and undergo activation-induced cell death (AICD) via either autocrine or paracrine apoptosis. (C) Immune privileged tissues, such as the eye and testis, express FasL that triggers apoptosis in lymphocytes expressing Fas as a mechanism to prevent massive exacerbation of inflammatory reactions. Similarly, many tumor cells express FasL during disease progression and eliminate tumor reactive T cells as a means of immune evasion.

Physiologic regulation of immune responses by Fas/FasL-induced apoptosis. (A) Activation of T cells by the engagement of T-cell receptors (TCR) with the peptide/major histocompatibility complex (MHC) bimolecular complex in conjunction with the transduction of secondary signals (not shown) leads to the up-regulation of both Fas and FasL expression. (B) Upon repeated antigenic stimulation, T cells become sensitive to Fas/FasL-mediated apoptosis and undergo activation-induced cell death (AICD) via either autocrine or paracrine apoptosis. (C) Immune privileged tissues, such as the eye and testis, express FasL that triggers apoptosis in lymphocytes expressing Fas as a mechanism to prevent massive exacerbation of inflammatory reactions. Similarly, many tumor cells express FasL during disease progression and eliminate tumor reactive T cells as a means of immune evasion.

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