Abstract:
:The ability of local ultraviolet B (UVB) irradiation to impair the induction of dinitrofluorobenzene (DNFB)-specific contact hypersensitivity (CH) in mice has been shown to be genetically determined. We have explored the possibility that the mouse Tnfa and Lps loci are involved. We demonstrate that C3H/HeN (Lpsn) strains are UVB-susceptible, whereas C3H/HeJ (Lpsd) strains are UVB-resistant. Our results indicate that local intradermal (ID) injection of mouse recombinant tumor necrosis factor-alpha (TNFa) into sites painted with DNFB impaired the induction of CH, and in a dose response experiment the effect was found to be more marked in C3H/HeN than in C3H/HeJ. Systemic administration of neutralizing TNFa-specific antibody reconstituted the UVB-induced defect in induction of CH in UVB-susceptible mice, confirming that TNFa is a major mediator of the deleterious effects of UVB on induction of cutaneous immunity. The UVB-susceptibility trait (revealed by effects on CH) correlates positively with a recently described restriction fragment length polymorphism (RFLP) at the Tnfa locus (allele b) and with the wild-type Lpsn allele. These results suggest that appropriate alleles at the Tnfa and Lps loci conspire to render mice susceptible to the impairment of CH induction by UVB. We propose that the mechanism may function through the capacity of UVB to elicit excessive local (cutaneous) production of TNFa, which mediates the immune defect.
journal_name
Immunogeneticsjournal_title
Immunogeneticsauthors
Yoshikawa T,Streilein JWdoi
10.1007/BF00241633subject
Has Abstractpub_date
1990-01-01 00:00:00pages
398-405issue
6eissn
0093-7711issn
1432-1211journal_volume
32pub_type
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