Tumor necrosis factor suppresses interleukin 10 in peripheral B cells via upregulating Bcl2‐like protein 12 in patients with inflammatory bowel disease | Zendy

Guo Xiutian | Zendy; Li MaoGang | Zendy; Li ShanShan | Zendy; Liu FengHua | Zendy; Liu ZhanJu | Zendy; Yang PingChang | Zendy

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Tumor necrosis factor suppresses interleukin 10 in peripheral B cells via upregulating Bcl2‐like protein 12 in patients with inflammatory bowel disease

Author(s) -

Guo Xiutian,

Li MaoGang,

Li ShanShan,

Liu FengHua,

Liu ZhanJu,

Yang PingChang

Publication year - 2017

Publication title -

cell biochemistry and function

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.933

H-Index - 61

eISSN - 1099-0844

pISSN - 0263-6484

DOI - 10.1002/cbf.3250

Subject(s) - tumor necrosis factor alpha , pathogenesis , immune system , immunology , interleukin , inflammatory bowel disease , interleukin 10 , blot , medicine , peripheral blood mononuclear cell , cytokine , biology , disease , gene , in vitro , biochemistry

The pathogenesis of the immune regulation dysfunction is unclear. Bcl2‐like protein 12 (Bcl2L12) has immune suppression function. This study tests a hypothesis that tumor necrosis factor (TNF) increases Bcl2L12 to suppress the expression of interleukin (IL) 10 in peripheral B cells of patients with inflammatory bowel disease (IBD). In this study, peripheral blood samples were collected from IBD patients and healthy controls. B cells were isolated from the blood samples. The expression of IL‐10 and Bcl2L12 in B cells was analyzed by quantitative reverse transcription polymerase chain reaction and Western blotting. We observed that the expression of Bcl2L12 in the peripheral B cells was higher in IBD patients than that in healthy controls. The IL‐10 levels in B cells were negatively correlated with the expression of Bcl2L12. Exposure of B cells to TNF in the culture enhanced the expression of Bcl2L12. The Bcl2L12 mediated the effects of TNF on suppression of IL‐10 in B cells. In conclusion, Bcl2L12 mediates the effects of TNF to suppress the expression of IL‐10 in B cells. The data suggest that Bcl2L12 may be a therapeutic target for the treatment of IBD.

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