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: Inhibition of IL-12 and IL-23 via TNF Receptor 1 in Macrophages and Dendritic Cells1
Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA 30322
IL-12 and TNF-
are central proinflammatory cytokines produced by macrophages and dendritic cells. Disregulation of TNF- is associated with sepsis and autoimmune diseases such as rheumatoid arthritis. However, new evidence suggests an anti-inflammatory role for TNF-. TNF--treated murine macrophages produced less IL-12p70 and IL-23, after stimulation with IFN-
and LPS. Frequency of IL-12p40-producing macrophages correspondingly decreased as measured by intracellular cytokine staining. IL-12p40 production was also inhibited in dendritic cells. TNFR1 was established as the main receptor involved in IL-12p40 regulation, because IL-12p40 levels were not affected by TNF- in TNFR1–/–-derived macrophages. Macrophages activated during Listeria monocytogenes infection were more susceptible to inhibition by TNF- than cells from naive animals, which suggests a regulatory role for TNF- in later stages of infection. This nonapoptotic anti-inflammatory regulation of IL-12 and IL-23 is an important addition to the multitude of TNF--induced responses determined by cell-specific receptor signaling.
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