Tumor necrosis factor-alpha impairs contact hypersensitivity induction after ultraviolet B radiation via TNF-receptor 2 ( p75).
Acute, low dose ultraviolet B radiation (UVR) impairs induction of contact hypersensitivity (CH) in genetically susceptible mice. Polymorphic alleles at the TNF-alpha locus dictate the susceptibility phenotype, and neutralizing anti-TNF-alpha antibodies restore CH induction in mice exposed to UVR. This circumstantial evidence strongly implicates TNF-alpha in the pathogenesis of failed CH induction after UVR. Using mice genetically deficient in TNF-receptor 1 (p55) or TNF-receptor 2 ( p75), we now report that the capacity of TNF-alpha to impair CH induction after UVR required signaling via TNF-receptor 2, rather than TNF-receptor 1. Moreover, acting via the same receptor, TNF-alpha altered the density and morphology of class II MHC-bearing epidermal Langerhans cells. However, UVR retained its capacity to induce tolerance in both TNF-receptor 1 and TNF-receptor 2 deficient mice, indicating that TNF-alpha plays no role in the systemic immune deficit created by UVR.[1]References
- Tumor necrosis factor-alpha impairs contact hypersensitivity induction after ultraviolet B radiation via TNF-receptor 2 (p75). Kurimoto, I., Streilein, J.W. Exp. Dermatol. (1999) [Pubmed]
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