Mycobacterium tuberculosis inhibits neutrophil apoptosis, leading to delayed activation of naïve CD4 T cells

Blomgran, R. et al. Cell Host & Microbe. 11, 81-90 (2012)

Speaker: Hsin-Pei Hsieh (謝欣倍)                                Time: 15:10~16:00, May 2, 2012

Commentator: Prof. Yee-Shin Lin (林以行老師)         Place: Room 601

Abstract

Mycobacterium tuberculosis (Mtb) is a human pathogen that causes death for more than 4000 people every day. Inhibition of macrophage apoptosis is one of the mechanisms to avoid host defense by M. tuberculosis¹. In this study, the authors intended to know whether the antiapoptoticmechanisms of M. tuberculosis exist in other myeloid cells during in vivo infection. Mice were infected with wild-type M. tuberculosis (H37Rv), and proapoptosis strain of M. tuberculosis (∆nuoG, virulence factor), respectively. By comparison with wild-type infection, the antiapoptotic ability of∆nuoG is not only limited in macrophages but also affects neutrophils and dendritic cells during early stage of infection. Apoptosis of neutrophlis accelerate antigen presentation to dendritic cells and subsequently activate CD4 T cells. Delayed proliferation of CD4 T cell was observed inneutrophlis depleted experiment and ∆nuoG infected mice. Likewise, inhibition of neutrophil apoptosis by H37Rv certainly contributes to delay CD4 T cells proliferate in vivo. In summary, M. tuberculosis suppresses neutrophils apoptosis, and delay dendriric cell present antigen to lymph node so that hinder timely activation and proliferation of naïve M. tuberculosis CD4 T cell.

Reference

1.      Behar, et al. Evasion of innate immunity by Mycobacterium tuberculosis: is death an exit strategy? Nat. Rev. Microbiol. 8, 668-674 (2010)