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Programmed Cell Death and AIDS Pathogenesis: Significance and Potential Mechanisms

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Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 200))

Abstract

Human immunodeficiency virus (HIV) infection leads, within about 10 years, to acquired immunodeficiency syndrome (AIDS), characterized by cell loss in several organs, including CD4+ T cells in the immune system, hematopoietic progenitors in the bone marrow and neurons in the brain (Everall et al. 1991; Fauci 1988, 1993; Levy 1993b). In the immune system, cell dysfunction is obseved before cell depletion is detected. These qualitative defects are characterized by a selective loss of CD4+ T cell memory function that includes, in vivo, a failure of CD4+ T cells to mediate delayed-type hypersensitivity reactions to self MHC class II-restricted recall antigens and, in vitro, a selective loss of the ability of T cells to proliferate in response to T cell receptor (TCR) stimulation by these recall antigens antibodies directed to the CD3/TCR complex, or defined polyclonal activators such as pokeweed mitogen (Clerici et al. 1989a,b; Hofmann et al. 1989; Lane et al. 1985; Miedema et al. 1988; Shearer et al. 1986). An additional and paradoxical feature of cell dysfunction in HIV-infected persons is the chronic activation state of the immune system, in spite of an apparent complete lack of CD4+ T helper (Th) cell function, that involves both HIV permissive (monocytes) and nonpermissive (B cells and CD8+T cells) cell populations (Fauci 1988,1993).

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Ameisen, J.C., Estaquier, J., Idziorek, T., De Bels, F. (1995). Programmed Cell Death and AIDS Pathogenesis: Significance and Potential Mechanisms. In: Kroemer, G., Martinez-A., C. (eds) Apoptosis in Immunology. Current Topics in Microbiology and Immunology, vol 200. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-79437-7_14

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