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Interleukin 35 may contribute to the loss of immunological self‐tolerance in patients with primary immune thrombocytopenia
Author(s) -
Sun Tiantian,
Zhang Donglei,
Yang Yanhui,
Zhang Xian,
Lv Cuicui,
Fu Rongfeng,
Lv Mingen,
Liu Wenjie,
Chen Yunfei,
Liu Wei,
Huang Yueting,
Xue Feng,
Liu Xiaofan,
Zhang Lei,
Li Huiyuan,
Yang Renchi
Publication year - 2015
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/bjh.13292
Subject(s) - immunology , immune thrombocytopenia , t cell , immune system , cd8 , medicine , interleukin , interleukin 10 , platelet , cytokine
Summary Primary immune thrombocytopenia ( ITP ) is an autoimmune disorder. Interleukin‐35 ( IL 35) can suppress T cell proliferation and elicit the development of inducible regulatory T cells (Tregs). Previous studies have shown decreased plasma IL 35 levels and dysfunctional T cells in patients with ITP . In this study, we determined whether decreased IL 35 levels correlate with T cell dysfunction in ITP patients. Plasma IL 35 levels were found to be lower in ITP patients than in healthy controls, were positively correlated with platelet levels and the percentage of peripheral circulating Tregs, and negatively correlated with the levels of T helper‐1 cells in ITP patients. We also evaluated the effects of IL 35 on cytokines contributing to T cell proliferation. IL 35 promoted the secretion of interleukin 10 ( IL 10) and transforming growth factor–β1 but reduced the levels of interferon‐γ and IL 17A (also termed IL 17). Moreover, IL 35 inhibited the proliferation of CD 4+ and CD 8+ T cells but induced the differentiation and proliferation of Tregs in ITP . In summary, IL 35 appears to contribute to the loss of immunological self‐tolerance in ITP patients by modulating T cells and immunoregulatory cytokines.