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Interleukin‐5 induces apoptotic defects in CD4 + T cells of patients with allergic rhinitis
Author(s) -
Luo XiangQian,
Ma Fei,
Wang Shuai,
Zhao MeiZhen,
Shao JianBo,
Geng XiaoRui,
Liu JiangQi,
Mo LiHua,
Guan Li,
Liu ZhiGang,
Liu DaBo,
Yang PingChang
Publication year - 2019
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.3a0718-287rr
Subject(s) - apoptosis , immune system , interleukin 21 , fas ligand , biology , immunology , microbiology and biotechnology , jurkat cells , pathogenesis , interleukin 4 , t cell , cancer research , programmed cell death , biochemistry
T helper (Th)2 polarization plays an important role in the pathogenesis of allergic diseases; the underlying mechanism remains to be further investigated. B cell lymphoma protein‐2 like protein‐12 (Bcl2L12) has the anti‐apoptotic function. This study aims to elucidate the contribution of Bcl2L12 to Th2 polarization in patients with allergic rhinitis (AR). In this study, human CD4 + T cells were isolated from blood samples collected from AR patients and healthy control (HC) subjects. The immune response profiles of CD4 + T cells were analyzed by immunologic approaches. The results showed that AR CD4 + T cells (CD4 + T cells collected from AR patients) showed defects of apoptosis. The expression of FasL in AR CD4 + T cells was lower than that of HC CD4 + T cells. Serum IL‐5 levels were negatively correlated with the expression of FasL in AR CD4 + T cells. Exposure of CD4 + T cells to IL‐5 in the culture suppressed the expression of FasL and increased the expression of Bcl2L12. IL‐5 increased the levels of Bcl2L12 in CD4 + T cells, the latter bound to the FasL promoter to prevent FasL gene transcription. Inhibition of Bcl2L12 restored the apoptosis machinery in AR CD4 + T cells. In conclusion, overexpression of Bcl2L12 in CD4 + T cells compromises the apoptosis machinery; the latter can be restored by inhibition of Bcl2L12. BcL2L12 in CD4 + T cells may be a novel target for the treatment of AR and other allergic disorders.