ESAT-6–dependent cytosolic pattern recognition drives noncognate tuberculosis control in vivo
Identifieur interne : 00E308 ( Main/Exploration ); précédent : 00E307; suivant : 00E309ESAT-6–dependent cytosolic pattern recognition drives noncognate tuberculosis control in vivo
Auteurs : Andreas Kupz [Allemagne, Australie] ; Ulrike Zedler [Allemagne] ; Manuela St Ber [Allemagne] ; Carolina Perdomo [Allemagne] ; Anca Dorhoi [Allemagne] ; Roland Brosch [France] ; Stefan H. E. Kaufmann [Allemagne]Source :
- The Journal of Clinical Investigation [ 0021-9738 ] ; ????.
Abstract
IFN-γ is a critical mediator of host defense against
Url:
DOI: 10.1172/JCI84978
PubMed: 27111234
PubMed Central: 4887189
Affiliations:
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<series><title level="j">The Journal of Clinical Investigation</title>
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<front><div type="abstract" xml:lang="en"><p>IFN-γ is a critical mediator of host defense against <italic>Mycobacterium tuberculosis</italic>
(<italic>Mtb</italic>
) infection. Antigen-specific CD4<sup>+</sup>
T cells have long been regarded as the main producer of IFN-γ in tuberculosis (TB), and CD4<sup>+</sup>
T cell immunity is the main target of current TB vaccine candidates. However, given the recent failures of such a TB vaccine candidate in clinical trials, strategies to harness CD4-independent mechanisms of protection should be included in future vaccine design. Here, we have reported that noncognate IFN-γ production by <italic>Mtb</italic>
antigen–independent memory CD8<sup>+</sup>
T cells and NK cells is protective during <italic>Mtb</italic>
infection and evaluated the mechanistic regulation of IFN-γ production by these cells in vivo. Transfer of arenavirus- or protein-specific CD8<sup>+</sup>
T cells or NK cells reduced the mortality and morbidity rates of mice highly susceptible to TB in an IFN-γ–dependent manner. Secretion of IFN-γ by these cell populations required IL-18, sensing of mycobacterial viability, <italic>Mtb</italic>
protein 6-kDa early secretory antigenic target–mediated (ESAT-6–mediated) cytosolic contact, and activation of NLR family pyrin domain–containing protein 3 (NLRP3) inflammasomes in CD11c<sup>+</sup>
cell subsets. Neutralization of IL-18 abrogated protection in susceptible recipient mice that had received noncognate cells. Moreover, improved <italic>Mycobacterium</italic>
<italic>bovis</italic>
bacillus Calmette-Guérin (BCG) vaccine–induced protection was lost in the absence of ESAT-6–dependent cytosolic contact. Our findings provide a comprehensive mechanistic framework for antigen-independent IFN-γ secretion in response to <italic>Mt</italic>
b with critical implications for future intervention strategies against TB.</p>
</div>
</front>
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<name sortKey="St Ber, Manuela" sort="St Ber, Manuela" uniqKey="St Ber M" first="Manuela" last="St Ber">Manuela St Ber</name>
<name sortKey="Zedler, Ulrike" sort="Zedler, Ulrike" uniqKey="Zedler U" first="Ulrike" last="Zedler">Ulrike Zedler</name>
</country>
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</country>
<country name="France"><region name="Île-de-France"><name sortKey="Brosch, Roland" sort="Brosch, Roland" uniqKey="Brosch R" first="Roland" last="Brosch">Roland Brosch</name>
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