Gene expression study of IL10 family genes in vitiligo skin biopsies, peripheral blood mononuclear cells and sera
Summary Background Vitiligo is a pigmentation disorder, the cause of which is complex and not yet fully understood. There is a significant change of epidermal cytokines in involved skin of patients with vitiligo compared with uninvolved skin and skin of healthy controls, thus suggesting a possible...
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Veröffentlicht in: | British journal of dermatology (1951) 2008-12, Vol.159 (6), p.1275-1281 |
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Sprache: | eng |
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Background Vitiligo is a pigmentation disorder, the cause of which is complex and not yet fully understood. There is a significant change of epidermal cytokines in involved skin of patients with vitiligo compared with uninvolved skin and skin of healthy controls, thus suggesting a possible involvement of cytokines in the pathogenesis of vitiligo.
Objectives To evaluate potential roles of IL10 family cytokines (IL10, IL19, IL20, IL22 and IL24) in vitiligo. Along with the selected cytokines, we investigated subunits of the receptors (IL10RA, IL10RB, IL20RA and IL22RA1) which are involved in the signalling pathway of the cytokines.
Methods Quantitative real‐time polymerase chain reaction was used to detect mRNA expression levels in samples extracted from skin biopsies and peripheral blood mononuclear cells and an enzyme‐linked immunosorbent assay was used to measure protein concentrations in serum from patients with vitiligo and healthy controls.
Results IL22 is significantly associated with vitiligo, especially with the active stage of vitiligo, as shown by results of mRNA expression and supported by results of protein level in sera. IL22 may provoke inflammation which leads to destruction of melanocytes.
Conclusions The actual role of IL22 during pathogenesis of vitiligo remains to be better characterized. Signal transductions of other investigated cytokines seem to be regulated on the expression level of their receptor complex subunits. |
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ISSN: | 0007-0963 1365-2133 |
DOI: | 10.1111/j.1365-2133.2008.08785.x |