作者
Alena M Gallegos, Jeroen WJ van Heijst, Miriam Samstein, Xiaodi Su, Eric G Pamer, Michael S Glickman
发表日期
2011/5/19
期刊
PLoS pathogens
卷号
7
期号
5
页码范围
e1002052
出版商
Public Library of Science
简介
CD4 T cell deficiency or defective IFNγ signaling render humans and mice highly susceptible to Mycobacterium tuberculosis (Mtb) infection. The prevailing model is that Th1 CD4 T cells produce IFNγ to activate bactericidal effector mechanisms of infected macrophages. Here we test this model by directly interrogating the effector functions of Th1 CD4 T cells required to control Mtb in vivo. While Th1 CD4 T cells specific for the Mtb antigen ESAT-6 restrict in vivo Mtb growth, this inhibition is independent of IFNγ or TNF and does not require the perforin or FAS effector pathways. Adoptive transfer of Th17 CD4 T cells specific for ESAT-6 partially inhibited Mtb growth while Th2 CD4 T cells were largely ineffective. These results imply a previously unrecognized IFNγ/TNF independent pathway that efficiently controls Mtb and suggest that optimization of this alternative effector function may provide new therapeutic avenues to combat Mtb through vaccination.
学术搜索中的文章
AM Gallegos, JWJ van Heijst, M Samstein, X Su… - PLoS pathogens, 2011