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Fas ligation on macrophages enhances IL-1R1- Toll-like receptor 4 signaling and promotes chronic inflammation.
The nonapoptotic functions of Fas ligation are incompletely characterized. In contrast to expectations, we show here that Fas-deficient mice developed less-severe collagen-induced arthritis than did control mice. Despite having milder arthritis, Fas-deficient mice had more of the critical pro-inflammatory mediator interleukin-1 beta ( IL-1 beta) in their joints, suggesting inefficient activation through IL-1 receptor 1 ( IL-1R1) when Fas signaling is deficient. In primary human macrophages and macrophages from Fas- or Fas ligand (FasL)-deficient mice, interruption of Fas-FasL signaling suppressed nuclear factor-kappa B activation and cytokine expression induced by IL-1 beta and lipopolysaccharide. This cross-talk was mediated by the Fas-associated death domain through interaction with myeloid differentiation factor 88. These observations document a unique mechanism whereby Fas-FasL interactions enhance activation through the IL-1R1 or Toll-like receptor 4 pathway, which may contribute to the pathogenesis of chronic arthritis.[1]References
- Fas ligation on macrophages enhances IL-1R1-Toll-like receptor 4 signaling and promotes chronic inflammation. Ma, Y., Liu, H., Tu-Rapp, H., Thiesen, H.J., Ibrahim, S.M., Cole, S.M., Pope, R.M. Nat. Immunol. (2004) [Pubmed]
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