Activation of the formyl peptide receptor by the HIV-derived peptide T-20 suppresses interleukin-12 p70 production by human monocytes.
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 G(i)-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-beta, and tumor necrosis factor-alpha 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. (Blood. 2001;97:3531-3536)[1]References
- Activation of the formyl peptide receptor by the HIV-derived peptide T-20 suppresses interleukin-12 p70 production by human monocytes. Braun, M.C., Wang, J.M., Lahey, E., Rabin, R.L., Kelsall, B.L. Blood (2001) [Pubmed]
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