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Blood, 1 June 2001, Vol. 97, No. 11, pp. 3531-3536
IMMUNOBIOLOGY
Activation of the formyl peptide receptor by the
HIV-derived peptide T-20 suppresses
interleukin-12 p70 production by human monocytes
Michael C. Braun,
Ji
Ming Wang,
Edward Lahey,
Ronald L. Rabin, and
Brian L. Kelsall
From the Immune Cell Interaction Unit, Mucosal Immunity
Section, and the Cytokine Biology Unit, Laboratory of Clinical
Investigation, National Institute of Allergy and Infectious Diseases,
National Institutes of Health, Bethesda; and the Laboratory of
Molecular Immunoregulation, Division of Basic Sciences, National Cancer
Institute-Frederick Cancer Research and Development Center, MD.
It has been proposed that in the early stages of human
immunodeficiency (HIV) infection, before the loss of CD4+ T
cells, inhibition of IL-12 production from host antigen-presenting cells plays a critical role in the suppression of T-helper cell type 1 responses. Activation of the Gi-protein-coupled
high-affinity N-formyl peptide receptor by f-met-leu-phe and
HIV-derived peptide T-20-suppressed IL-12 p70 production from human
monocytes in response to both T-cell-dependent and T-cell-independent
stimulation are reported. Activation of the low-affinity N-formyl
peptide receptor by the HIV-derived F-peptide suppressed IL-12
production more modestly. This suppression was pertussis toxin
sensitive and was selective for IL-12; the production of IL-10,
transforming growth factor- , and tumor necrosis factor- was
unaltered. The production of IL-12 p70 by dendritic cells was
unaffected by these peptides despite functional expression of the
high-affinity fMLP receptor. These findings provide a potential direct
mechanism for HIV-mediated suppression of IL-12 production and suggest
a broader role for G-protein-coupled receptors in the regulation of
innate immune responses.
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