Transcription-coupled and global genome repair differentially influence UV-B-induced acute skin effects and syste
2000
Exposure to UV-B radiation impairs immune responses in mammals by
inhibiting especially Th1-mediated contact hypersensitivity and
delayed-type hypersensitivity. Immunomodulation is not restricted to the
exposed skin, but is also observed at distant sites, indicating the
existence of mediating factors such as products from exposed skin cells or
photoactivated factors present in the superficial layers. DNA damage
appears to play a key role, because enhanced nucleotide excision repair
(NER) strongly counteracts immunosuppression. To determine the effects of
the type and genomic location of UV-induced DNA damage on
immunosuppression and acute skin reactions (edema and erythema) four
congenic mouse strains carrying different defects in NER were compared:
CSB and XPC mice lacking transcription-coupled or global genome NER,
respectively, as well as XPA and TTD/XPD mice carrying complete or partial
defects in both NER subpathways, respectively. The major conclusions are
that 1) transcription-coupled DNA repair is the dominant determinant in
protection against acute skin effects; 2) systemic immunomodulation is
only affected when both NER subpathways are compromised; and 3) sunburn is
not related to UV-B-induced immunosuppression.
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