例如:"lncRNA", "apoptosis", "WRKY"

Chlamydia muridarum infection induces CD4+ T cells apoptosis via PI3K/AKT signal pathway.

Pathog Dis. 2019 Apr 01;77(3)
Ningbo Zheng 1 , Lida Sun 1 , Gaoju Pang 1 , Xiaoyu Zha 1 , Wenhao Niu 1 , Lu Tan 1 , Hong Zhang 1 , Hong Bai 1
Ningbo Zheng 1 , Lida Sun 1 , Gaoju Pang 1 , Xiaoyu Zha 1 , Wenhao Niu 1 , Lu Tan 1 , Hong Zhang 1 , Hong Bai 1
+ et al

[No authors listed]

Author information
  • 1 Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Educational Ministry of China, No.22 Qixiangtai Road, Heping District, Tianjin, 300070, China.

摘要


Apoptosis is essential for the homeostatic control of the lymphocytes number during the development of an immune response to an invasive microorganism. CD4+ T cells play a major role in homeostasis of the immune system and are sufficient to confer protection against Chlamydia muridarum (Cm) infection in mice. The present study demonstrated that phosphatidylinositol 3-kinase (PI3K) p110δ mRNA and phosphorylation of protein kinase B (p-AKT) level were significantly increased in lung cells and spleen cells at day 3 and day 7 post-infection, p-AKT level was inhibited when adding PI3K inhibitor LY294002. Moreover, Cm infection induced high levels of IL-2/IL-2Rα in CD4+ T cells, which may relate to PI3K/AKT signal pathway activation. We observed that Cm infection significantly induced apoptosis of CD4+ T cells. The related apoptosis proteins Bcl-2 and Mcl-1 uneven expression levels were induced in CD4+ T cells by Cm infection. These findings provided in vivo and in vitro evidence that Cm infection induces CD4+ T cells apoptosis possibly via PI3K/AKT signal pathway.

KEYWORDS: Chlamydia muridarum , Bcl-2/Bax/Mcl-1, CD4+ T cells, IL-2, PI3K/AKT, apoptosis