Premium
A single sub‐erythematous exposure of solar‐simulated radiation on the elicitation phase of contact hypersensitivity induces IL‐10‐producing T‐regulatory cells in human skin
Author(s) -
Stoebner Pierre E.,
Rahmoun Massilva,
Ferrand Christophe,
Meunier Laurent,
Yssel Hans,
Pène Jérôme
Publication year - 2006
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2006.00452.x
Subject(s) - immunology , t cell receptor , immunosuppression , allergic contact dermatitis , t cell , antigen presenting cell , chemistry , allergy , medicine , immune system
Solar ultraviolet (UV) radiation has hazardous effects on human health that are, in part, associated with its immunosuppressive effects via the induction of interleukin (IL)‐10 production. Although IL‐10 is produced by both T helper type 2 (Th2) cells and T‐regulatory type 1 (Tr1) cells, the relative contribution of either subset in UV radiation‐induced immunosuppression has not been established. Here, we show that T cells isolated from non‐treated allergic contact dermatitis (ACD) reactions, 48 h following nickel challenge and propagated for 7–10 days in the presence of IL‐2, were mainly CD4 + and produced IL‐10, but little interferon‐ γ . A single sub‐erythematous solar‐simulated radiation (SSR) prior to antigen challenge exposure resulted in a clinical attenuation of the intensity of ACD reactions which was associated with a significant increase in both the magnitude of IL‐10 production by skin‐infiltrating T cells and the frequency of IL‐10‐producing Tr1 cells. Skin‐infiltrating T cells in SSR‐exposed, as well as non‐exposed, ACD reactions showed a perturbed T‐cell receptor (TCR)‐V β repertoire, without overexpression of a particular TCR‐V β gene product, indicating the presence of high frequencies of nickel non‐specific T cells in ACD reactions. These results show that a single sub‐erythematous SSR induces immunosuppression via the cutaneous infiltration of IL‐10‐producing Tr1, and to a lesser extent, Th2 cells.