The Wistar Institute, Philadelphia, Pennsylvania
Correspondence: Dr. L. J. Montaner, Director HIV-1 Immunopathogenesis Lab, The Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104. E-mail: montaner{at}wistar.upenn.edu
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 ß, interferon-
/ß,
tumor necrosis factor , 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.
Key Words: transforming growth factor ß • interferon • tumor necrosis factor
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