Premium
Ultraviolet B radiation exerts enhancing effects on the production of a complement component, C3, by interferon‐γ‐stimulated cultured human epidermal keratinocytes, in contrast to photochemotherapy and ultraviolet A radiation that show suppressive effects
Author(s) -
Terui T.,
Funayama M.,
Terunuma A.,
Takahashi K.,
Tagami H.
Publication year - 2000
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1046/j.1365-2133.2000.03410.x
Subject(s) - psoriasis , puva therapy , phototoxicity , interferon gamma , epidermis (zoology) , psoralen , interferon , dermatology , chemistry , immunology , microbiology and biotechnology , medicine , biology , cytokine , in vitro , biochemistry , anatomy , dna
The present study was designed to investigate by using enzyme‐linked immunosorbent assay and reverse transcriptase–polymerase chain reaction methods whether photochemotherapy (PUVA) or ultraviolet (UV) B treatment affects C3 production by interferon (IFN)‐γ‐stimulated keratinocytes cultured in serum‐free medium. The results showed that PUVA and UVA reduced C3 production by IFN‐γ‐stimulated epidermal keratinocytes dose‐dependently, although the effect of PUVA was stronger than that of UVA alone. Interestingly, UVB induced an enhancement of C3 production at doses ranging from 10 to 50 mJ cm −2 . This phenomenon was found at both the protein and mRNA levels. In every experiment, changes in C3 mRNA levels preceded those in its protein levels. Reduced C3 production at higher doses of 75 and 100 mJ cm −2 were probably due to cytotoxic effects of UVB. In our experimental system, PUVA, UVA or UVB treatment did not affect C3 production without IFN‐γ stimulation. Our results suggest that a reduction in C3 production by PUVA treatment may in part explain the efficacy of PUVA in the treatment of inflammatory dermatoses such as psoriasis, while the results of the UVB experiments may partially explain the proinflammatory nature of UVB.