Proinflammatory response and IL-12 expression in HIV-1 infection.
HIV-1 infection elicits a broad range of host responses, many of which interfere with the regulatory pathways of gene expression of interleukin-12 (IL-12), a heterodimeric cytokine essential for cell-mediated immunity against microbial infection. The inhibition of IL-12 production by accessory cells after HIV-1 infection has been identified as a potential factor responsible for impaired innate and Th1 cell-mediated responses observed in AIDS patients. The mechanism by which HIV-1 infection suppresses IL-12 gene expression is largely uncharacterized. Here we review all pathways identified that could potentially mediate HIV-induced impairment of IL-12 gene expression, such as IL-10, transforming growth factor beta, interferon-alpha/beta, tumor necrosis factor alpha, Fc receptors, complement regulatory proteins, and receptors. Also discussed is the decreased CD40 ligand induction in CD4 T cells during HIV infection, which may have a strong impact on T cell-dependent IL-12 production that is critical for the establishment and maintenance of a Th1 response.
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The Wistar Institute, Philadelphia, Pennsylvania 19104, USA.
Montaner
L J
LJ
D000818:Animals; D005786:Gene Expression Regulation / Q000502:physiology; D015658:HIV Infections / Q000276:immunology / Q000378:metabolism*; D015497:HIV-1; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000378:metabolism; D018664:Interleukin-12 / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology
D018664:Interleukin-12