Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/24312
Title: Ultraviolet B induced suppression of induction of contact sensitivity in human skin is not associated with tumour necrosis factor-alpha-308 or interleukin-10 genetic polymorphisms
Authors: Allen, M. H.
Barker, J. N. W. N.
Skov, L.
Baadsgaard, O.
Barber, R.
Trembath, R.
Simon, J.
First Published: Aug-1998
Publisher: Wiley, British Association of Dermatologists
Citation: British Journal of Dermatology, 1998, 139 (2), pp. 225-229
Abstract: Low doses of ultraviolet B (UVB) can induce localized immunosuppression in skin. This effect may be important in the induction of skin cancers and is thought to be mediated by tumour necrosis factor (TNF) α and interleukin (IL) 10 in conjunction with other factors. In humans a transition polymorphism in the TNF-α gene may affect TNF-α secretion and the promoter region of the IL-10 gene contains a CA repeat polymorphism which may affect gene function. We have therefore investigated the association of these polymorphisms with UVB-induced immunosuppression in humans. Volunteers (n = 42) were irradiated with UVB then sensitized on irradiated skin with diphenylcyclopropanone (DPCP) and subsequently antigen challenged with DPCP. DNA was extracted from blood samples and volunteers genotyped for the TNF-α polymorphism by polymerase chain reaction (PCR) and restriction digestion. The CA repeat polymorphism was amplified by PCR and sized by gel electrophoresis. Twenty-four volunteers were susceptible to UVB-induced immunosuppression and 18 were resistant. The association of allele frequencies and phenotype was statistically tested using a χ2-test. For both the TNF-α and IL-10 polymorphisms, there was no statistically significant association between allele types and response to UVB. These results indicate that variation in the immune response to UVB in humans is not associated with the TNF-α-308 transition or IL-10 CA repeat polymorphisms, although other as yet undetected DNA sequence variants of these genes may be involved.
DOI Link: 10.1046/j.1365-2133.1998.02358.x
ISSN: 0007-0963
eISSN: 1365-2133
Links: http://hdl.handle.net/2381/24312
http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2133.1998.02358.x/abstract
Type: Journal Article
Appears in Collections:Published Articles, Dept. of Genetics

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