ISSN:
1600-0625
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
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.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1600-0625.1999.tb00308.x
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