ISSN:
0021-9541
Keywords:
Life and Medical Sciences
;
Cell & Developmental Biology
Source:
Wiley InterScience Backfile Collection 1832-2000
Topics:
Biology
,
Medicine
Notes:
Ultraviolet light A (UVA) is shown to play an augmentative or synergistic role with UVB in pathophysiological conditions induced by solar radiation. Thus, UVA would contribute significantly to the development of skin malignancies. It remains unclear, however, how UVA contributes to solar radiation-induced immune suppression. Keratinocytes (KC) produce cytokines which are a significant mediator of inflammatory and immunologic reactions in skin exposed to solar radiation and are a potent mediator in the induction of immune suppression. To examine if UVA alters the expression and production of cytokines from KC, normal human keratinocytes (HuSK) were cultured and exposed to UVA at doses ranging between 2.5 and 20 kJ/m2. Constitutive expression of the p35 subunit of interleukin (IL)-12 was detected by reverse transcription-polymerase chain reaction (RT-PCR) and the p40 subunit was induced by UVA irradiation dose dependently. IL-12 protein was also detected in the supernatants from UVA-irradiated HuSK by enzyme-linked imuunosorbent assay (ELISA) and confirmed by a bioassay. On the other hand, the same doses of UVA did not induce IL-10 mRNA or IL-10 protein which has been shown to be one of the cytokines responsible for the induction of UVB-induced immunosuppression. Considering that IL-12 promotes activation of Th1 cells and prevents the activation of Th2 cells and that administration of IL-12 has been shown to block the induction of immune suppression in UV-irradiated animals, our results suggest that UVA modulates skin immune function distinctively from UVB by affecting the balance between IL-10 and IL-12 produced from KC. J. Cell. Physiol. 177:493-498, 1998. © 1998 Wiley-Liss, Inc.
Additional Material:
7 Ill.
Type of Medium:
Electronic Resource
