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

Overview

abstract

  • 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.

publication date

  • September 1, 2000

Research

keywords

  • HIV Infections
  • HIV-1
  • Interleukin-12

Identity

Scopus Document Identifier

  • 0033637535

PubMed ID

  • 10985255

Additional Document Info

volume

  • 68

issue

  • 3