Human innate Mycobacterium tuberculosis-reactive alphabetaTCR+ thymocytes.

The control of Mycobacterium tuberculosis (Mtb) infection is heavily dependent on the adaptive Th1 cellular immune response. Paradoxically, optimal priming of the Th1 response requires activation of priming dendritic cells with Th1 cytokine IFN-gamma. At present, the innate cellular mechanisms requi...

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書目詳細資料
發表在:PLoS Pathogens
Main Authors: Marielle C Gold, Heather D Ehlinger, Matthew S Cook, Susan K Smyk-Pearson, Paul T Wille, Ross M Ungerleider, Deborah A Lewinsohn, David M Lewinsohn
格式: Article
語言:英语
出版: Public Library of Science (PLoS) 2008-02-01
在線閱讀:http://europepmc.org/articles/PMC2242840?pdf=render
實物特徵
總結:The control of Mycobacterium tuberculosis (Mtb) infection is heavily dependent on the adaptive Th1 cellular immune response. Paradoxically, optimal priming of the Th1 response requires activation of priming dendritic cells with Th1 cytokine IFN-gamma. At present, the innate cellular mechanisms required for the generation of an optimal Th1 T cell response remain poorly characterized. We hypothesized that innate Mtb-reactive T cells provide an early source of IFN-gamma to fully activate Mtb-exposed dendritic cells. Here, we report the identification of a novel population of Mtb-reactive CD4(-) alphabetaTCR(+) innate thymocytes. These cells are present at high frequencies, respond to Mtb-infected cells by producing IFN-gamma directly ex vivo, and display characteristics of effector memory T cells. This novel innate population of Mtb-reactive T cells will drive further investigation into the role of these cells in the containment of Mtb following infectious exposure. Furthermore, this is the first demonstration of a human innate pathogen-specific alphabetaTCR(+) T cell and is likely to inspire further investigation into innate T cells recognizing other important human pathogens.
ISSN:1553-7366
1553-7374