Abstract
Fas-mediated apoptosis contributes to physiological and pathological cellular processes, such as differentiation and survival. In particular, the roles of Fas in immune cells are complex and critical for the maintenance of immune tolerance. The precise pathways and unique functions associated with Fas/FasL-mediated signaling in the immune system are known. The dual character of Fas/FasL-mediated immune regulation that induces beneficial or harmful effects is associated with the onset or development of immune disorders. Studies on mutations in genes encoding Fas and FasL gene of humans and mice contributed to our understanding of the pathogenesis of autoimmune diseases. Here, we review the opposing functions of Fas/FasL-mediated signaling, bilateral effects of Fas/FasL on in immune cells, and complex pathogenesis of autoimmunity mediated by Fas/FasL.
Highlights
Fas receptor (CD95, tumor necrosis factor receptor superfamily member 6) is a death receptor (DR) localized on the surface of various cells, which triggers a signal transduction pathway leading to apoptosis [1, 2]
These results suggest that killer B cells induced by viral infections and tumor cells play a crucial role in the ability of virus-infected or cancer cells to evade the host’s immune system
B cell-specific Fas deficiency is associated with the onset of autoimmunity [60], suggesting that Fas prevents the development of self-reactive germinal center (GC) B cells that escape normal regulatory controls and produce high amounts of immunoglobulin and autoantibodies [60, 61]
Summary
Fas receptor (CD95, tumor necrosis factor receptor superfamily member 6) is a death receptor (DR) localized on the surface of various cells, which triggers a signal transduction pathway leading to apoptosis [1, 2]. FasL expression frequently occurs in patients with the aggressive form of B-CLL as well as in other human B-cell leukemias and lymphomas, most notably, multiple myeloma [58, 59] These results suggest that killer B cells induced by viral infections and tumor cells play a crucial role in the ability of virus-infected or cancer cells to evade the host’s immune system. MRL-lpr/lpr mice produce circulating autoantibodies, such as rheumatoid factor as well as those against a single- and double-strand DNA and nuclear antigens [62, 63], indicating the contribution of FasL/Fas signaling in B cells to cellular processes such as differentiation, proliferation, death, and immunoglobulin production. Fas signal in B cell plays potent roles in the function and the pathogenesis of immune disorders
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