期刊
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
卷 564, 期 -, 页码 184-188出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2014.10.004
关键词
T lymphocyte; Apoptosis; Fas ligand; Chromobox homolog 7; Methylation
资金
- National Nature Science Found of China [81273204]
- National Natural Science Fund for Youth of China [81400240]
- Shanghai Health and Family Planning Commission Scientific Reseach Project [201440632]
- National Nature Science Found for Youth of China [81100721]
- Zhuoxue Plan Funds of the Fudan University
CD4(+) T cell polarization plays a critical role in a number of immune disorders; the pathogenesis is unclear. Chromobox homolog 7 (Cbx7) is involved in the gene transcription of several cell types. This study aims to investigate the mechanism by which Cbx7 modulates the CD4(+) T cell polarization. Expression of Cbx7 was assessed by quantitative RT-PCR and Western blotting. Apoptosis of CD4(+) T cell was analyzed by flow cytometry. The FasL promoter methylation was evaluated by the methylation specific PCR. The results showed that CD4(+) CD25(-) T cells express Cbx7 that was increased significantly after activation by exposing to anti-CD3/CD28 Ab, but suppressed by exposing to specific antigens. More apoptotic cells were detected in CD4(+) T cells with the Cbx7 gene knockdown. Exposure to insulin-like growth factor-1 up regulated the expression of Cbx7 in CD4(+) T cells. After antigen-specific TCR activation, Cbx7-deficient CD4(+) T cells expressed more FasL and showed the FasL gene promoter hyper demethylation than wild CD4(+) T cells. In addition, CD4(+) T cells with overexpression of Cbx7 showed lower levels of FasL gene promoter demethylation. We conclude that CD4(+) T cells express Cbx7; the latter prevents FasL expression and the activation-induced CD4(+) T cell apoptosis. (C) 2014 Elsevier Inc. All rights reserved.
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