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Tumor necrosis factor‐alpha impairs contact hypersensitivity induction after ultraviolet B radiation via TNF‐receptor 2 (p75)
Author(s) -
Kurimoto I.,
Streilein J. W.
Publication year - 1999
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.1999.tb00308.x
Subject(s) - tumor necrosis factor alpha , receptor , immunology , biology , microbiology and biotechnology , genetics
Acute, low dose ultraviolet B radiation (UVR) impairs induction of contact hypersensitivity (CH) in genetically susceptible mice. Polymorphic alleles at the TNF‐α locus dictate the susceptibility phenotype, and neutralizing anti‐TNF‐α antibodies restore CH induction in mice exposed to UVR. This circumstantial evidence strongly implicates TNF‐α 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‐α to impair CH induction after UVR required signaling via TNF‐receptor 2, rather than TNF‐receptor 1. Moreover, acting via the same receptor, TNF‐α 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‐α plays no role in the systemic immune deficit created by UVR.