Pregnancy, HLA allogeneic challenge, and implications for AIDS etiology

Abstract 

Because of the large HLA genetic polymorphism, a human fetus usually has several paternal HLA antigens allogeneic to its mother. The maternal γ-immunoglobulin (IgG) antibody response to fetal HLA alloantigens is noncytotoxic and associated with local suppression of maternal cell-mediated immunity (CMI) at the maternal–fetal interface. When mother and fetus are syngeneic for most HLA antigens, an increased risk exists for a maternal anti-placental cytotoxic CMI responses, compromising fetal survival. Local suppression of maternal CMI by an anti-HLA IgG response may have evolved to protect the fetoplacental unit from a maternal CMI cytotoxic reaction against expressed developmental neoantigens. A negative aspect of this adaptive response is that infectious organisms bearing HLA-homologous alloantigens (e.g. human immunodeficiency virus type 1, HIV-1) may generate a systemic IgG response suppressing CMI. Findings are reviewed suggesting this is an etiologic factor in the acquired immune deficiency syndrome (AIDS).

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