首页> 中文期刊> 《生物医学与环境科学:英文版》 >Novel Protein C6ORF120 Promotes Apoptosis through Mitochondria-dependent Pathway in CD4+ T Lymphocytes

Novel Protein C6ORF120 Promotes Apoptosis through Mitochondria-dependent Pathway in CD4+ T Lymphocytes

         

摘要

Generally,a healthy immune system should be in dynamic balance,which can be maintained by both promoting and resisting inflammation.Lymphocyte apoptosis is indispensable for maintaining homeostasis[1]and participates in the entire process of lymphocyte differentiation,development,maturation,and immune effects.It has been reported that a large amount of lymphocyte apoptosis occurs in lymphoid organs during severe trauma[2].Lymphocytes consist of T and B lymphocytes,among which CD4^(+)T cells were the focus of this study.CD4^(+)T lymphocytes play an important role in the innate immunity.Apoptosis of CD4^(+)T lymphocytes is an important biological process that induces CD4^(+)T cell depletion[3].Numerous studies have shown that CD4^(+)T cell apoptosis participates in many pathological processes of diseases such as HIV infection,cancer,and systemic sclerosis[4].Classical apoptosis is induced by factors that can activate several pathways,including the mitochondrial,endoplasmic reticulum,and death receptor pathways[5].The mitochondrial pathway is mainly activated by the Bcl-2 family[6].The endoplasmic reticulum(ER)pathway is affected by endoplasmic reticulum disorders.Some external factors can trigger the death receptor pathway,such as the binding of TNF-TNFR and the combination of Fas-FasL[7].Considering these pathways,it is feasible to study the specific mechanisms of lymphocyte apoptosis,primarily in CD4^(+)T cells.

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