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Interleukin-17-dependent CXCL13 mediates mucosal vaccine-induced immunity against tuberculosis.


ABSTRACT: The variable efficacy of tuberculosis (TB) vaccines and the emergence of drug-resistant strains of Mycobacterium tuberculosis (Mtb) emphasize the urgency for not only generating new and more effective vaccines against TB but also understanding the underlying mechanisms that mediate vaccine-induced protection. We demonstrate that mucosal adjuvants, such as type II heat labile enterotoxin (LT-IIb), delivered through the mucosal route induce pulmonary Mtb-specific T helper type 17 (Th17) responses and provide vaccine-induced protection against Mtb infection. Importantly, protection is interferon-? (IFN?)-independent but interleukin-17 (IL-17)-dependent. Our data show that IL-17 mediates C-X-C motif chemokine ligand 13 (CXCL13) induction in the lung for strategic localization of proinflammatory cytokine-producing CXCR5+ (C-X-C motif chemokine receptor 5-positive) T cells within lymphoid structures, thereby promoting early and efficient macrophage activation and the control of Mtb. Our studies highlight the potential value of targeting the IL-17-CXCL13 pathway rather than the IFN? pathway as a new strategy to improve mucosal vaccines against TB.

SUBMITTER: Gopal R 

PROVIDER: S-EPMC3732523 | biostudies-literature | 2013 Sep

REPOSITORIES: biostudies-literature

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Interleukin-17-dependent CXCL13 mediates mucosal vaccine-induced immunity against tuberculosis.

Gopal R R   Rangel-Moreno J J   Slight S S   Lin Y Y   Nawar H F HF   Fallert Junecko B A BA   Reinhart T A TA   Kolls J J   Randall T D TD   Connell T D TD   Khader S A SA  

Mucosal immunology 20130109 5


The variable efficacy of tuberculosis (TB) vaccines and the emergence of drug-resistant strains of Mycobacterium tuberculosis (Mtb) emphasize the urgency for not only generating new and more effective vaccines against TB but also understanding the underlying mechanisms that mediate vaccine-induced protection. We demonstrate that mucosal adjuvants, such as type II heat labile enterotoxin (LT-IIb), delivered through the mucosal route induce pulmonary Mtb-specific T helper type 17 (Th17) responses  ...[more]

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