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Levels and function of regulatory T cells in patients with polymorphic light eruption: relation to photohardening
Author(s) -
Schweintzger N.,
GruberWackernagel A.,
Reginato E.,
Bambach I.,
Quehenberger F.,
Byrne S.N.,
Wolf P.
Publication year - 2015
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 - 10.1111/bjd.13930
Subject(s) - foxp3 , interleukin 7 receptor , flow cytometry , effector , immunology , il 2 receptor , medicine , regulatory t cell , t cell , immune system
Summary Background We hypothesized that regulatory T cells (Tregs) are involved in the immunological abnormalities seen in patients with polymorphic light eruption ( PLE ). Objectives To investigate the number and suppressive function of peripheral Tregs in patients with PLE compared with healthy controls. Methods Blood sampling was done in 30 patients with PLE [seeking or not seeking 311‐nm ultraviolet ( UV )B photohardening] as well as 19 healthy controls at two time points: TP 1, March to June (before phototherapy); and TP 2, May to August (after phototherapy). We compared the number of CD 4 + CD 25 high CD 127 − FoxP3 + Tregs by flow cytometry and their function by assessing FoxP3 mRNA levels and effector T cell/Treg suppression assays. Results Tregs isolated from healthy controls significantly suppressed the proliferation of effector T cells at TP 1 by 68% ( P = 0·0156). In contrast, Tregs from patients with PLE entirely lacked the capacity to suppress effector T‐cell proliferation at that time point. The medical photohardening seen in 23 patients with PLE resulted in a significant increase in the median percentage of circulating Tregs [both as a proportion of all lymphocytes; 65 6% increase ( P = 0·0049), and as a proportion of CD 4 + T cells; 32.5% increase ( P = 0·0049)]. This was accompanied by an increase in the expression of FoxP3 mRNA ( P = 0·0083) and relative immunosuppressive function of Tregs ( P = 0·083) comparing the two time points in representative subsets of patients with healthy controls tested. Seven patients with PLE not receiving 311‐nm UVB also exhibited an increase in the number of Tregs but this was not statistically significant. No significant differences in Treg numbers were observed in healthy subjects between the two time points. Conclusions An impaired Treg function is likely to play a role in PLE pathogenesis. A UV ‐induced increase in the number of Tregs (either naturally or therapeutically) may be a compensatory mechanism by which the immune system counteracts the susceptibility to PLE .