scholarly journals Involvement of IL‐17A‐producing TCR γδ T cells in late protective immunity against pulmonary Mycobacterium tuberculosis infection

2016 ◽  
Vol 4 (4) ◽  
pp. 401-412 ◽  
Author(s):  
Masayuki Umemura ◽  
Yuko Okamoto‐Yoshida ◽  
Ayano Yahagi ◽  
Seigo Touyama ◽  
Susumu Nakae ◽  
...  
2018 ◽  
Vol 14 (8) ◽  
pp. e1007266 ◽  
Author(s):  
Shengfeng Hu ◽  
Xialin Du ◽  
Yulan Huang ◽  
Yuling Fu ◽  
Yalong Yang ◽  
...  

2014 ◽  
Vol 192 (7) ◽  
pp. 2965-2969 ◽  
Author(s):  
Shunsuke Sakai ◽  
Keith D. Kauffman ◽  
Jason M. Schenkel ◽  
Cortez C. McBerry ◽  
Katrin D. Mayer-Barber ◽  
...  

2010 ◽  
Vol 40 (8) ◽  
pp. 2211-2220 ◽  
Author(s):  
Nadia Caccamo ◽  
Giuliana Guggino ◽  
Simone A. Joosten ◽  
Giuseppe Gelsomino ◽  
Paola Di Carlo ◽  
...  

2008 ◽  
Vol 76 (5) ◽  
pp. 2249-2255 ◽  
Author(s):  
Ying Wu ◽  
Joshua S. Woodworth ◽  
Daniel S. Shin ◽  
Sheldon Morris ◽  
Samuel M. Behar

ABSTRACT The 10-kDa culture filtrate protein (CFP-10) and 6-kDa early secretory antigen of T cells (ESAT-6) are secreted in abundance by Mycobacterium tuberculosis and are frequently recognized by T cells from infected people. The genes encoding these proteins have been deleted from the genome of the vaccine strain Mycobacterium bovis bacillus Calmette-Guérin (BCG), and it is hypothesized that these proteins are important targets of protective immunity. Indeed, vaccination with ESAT-6 elicits protective CD4+ T cells in C57BL/6 mice. We have previously shown that M. tuberculosis infection of C3H mice elicits CFP-10-specific CD8+ and CD4+ T cells. Here we demonstrate that immunization with a CFP-10 DNA vaccine stimulates a specific T-cell response only to the H-2Kk-restricted epitope CFP-1032-39. These CFP-1032-39-specific CD8+ cells undergo a rapid expansion and accumulate in the lung following challenge of immunized mice with aerosolized M. tuberculosis. Protective immunity is induced by CFP-10 DNA vaccination as measured by a CFU reduction in the lung and spleen 4 and 8 weeks after challenge with M. tuberculosis. These data demonstrate that CFP-10 is a protective antigen and that CFP-1032-39-specific CD8+ T cells elicited by vaccination are sufficient to mediate protection against tuberculosis.


2010 ◽  
Vol 107 (45) ◽  
pp. 19408-19413 ◽  
Author(s):  
W. W. Reiley ◽  
S. Shafiani ◽  
S. T. Wittmer ◽  
G. Tucker-Heard ◽  
J. J. Moon ◽  
...  

2007 ◽  
Vol 76 (1) ◽  
pp. 426-436 ◽  
Author(s):  
Dan Huang ◽  
Yun Shen ◽  
Liyou Qiu ◽  
Crystal Y. Chen ◽  
Ling Shen ◽  
...  

ABSTRACT Little is known about the immune distribution and localization of antigen-specific T cells in mucosal interfaces of tissues/organs during infection of humans. In this study, we made use of a macaque model of Mycobacterium tuberculosis infection to assess phosphoantigen-specific Vγ2Vδ2 T cells regarding their tissue distribution, anatomical localization, and correlation with the presence or absence of tuberculosis (TB) lesions in lymphoid and nonlymphoid organs/tissues in the progression of severe pulmonary TB. Progression of pulmonary M. tuberculosis infection generated diverse distribution patterns of Vγ2Vδ2 T cells, with remarkable accumulation of these cells in lungs, bronchial lymph nodes, spleens, and remote nonlymphoid organs but not in blood. Increased numbers of Vγ2Vδ2 T cells in tissues were associated with M. tuberculosis infection but were independent of the severity of TB lesions. In lungs with apparent TB lesions, Vγ2Vδ2 T cells were present within TB granulomas. In extrathoracic organs, Vγ2Vδ2 T cells were localized in the interstitial compartment of nonlymphoid tissues, and the interstitial localization was present despite the absence of detectable TB lesions. Finally, Vγ2Vδ2 T cells accumulated in tissues appeared to possess cytokine production function, since granzyme B was detectable in the γδ T cells present within granulomas. Thus, clonally expanded Vγ2Vδ2 T cells appeared to undergo trans-endothelial migration, interstitial localization, and granuloma infiltration as immune responses to M. tuberculosis infection.


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