Proinflammatory response and IL-12 expression in HIV-1 infection.

TitleProinflammatory response and IL-12 expression in HIV-1 infection.
Publication TypeJournal Article
Year of Publication2000
AuthorsMa X, Montaner LJ
JournalJ Leukoc Biol
Date Published2000 Sep
KeywordsAnimals, Gene Expression Regulation, HIV Infections, HIV-1, Humans, Inflammation, Interleukin-12

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.

Alternate JournalJ Leukoc Biol
PubMed ID10985255
Grant ListAI40379 / AI / NIAID NIH HHS / United States
AI45899 / AI / NIAID NIH HHS / United States
CA79772 / CA / NCI NIH HHS / United States

Weill Cornell Medicine Microbiology and Immunology 1300 York Avenue, Box 62 New York, NY 10065 Phone: (212) 746-6505 Fax: (212) 746-8587