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Cutting edge: adaptive versus innate receptor signals selectively control the pool sizes of murine IFN-?- or IL-17-producing ?? T cells upon infection.


ABSTRACT: ?? T lymphocytes are commonly viewed as embracing properties of both adaptive and innate immunity. Contributing to this is their responsiveness to pathogen products, either with or without the involvement of the TCR and its coreceptors. This study clarifies this paradoxical behavior by showing that these two modes of responsiveness are the properties of two discrete sets of murine lymphoid ?? T cells. Thus, MyD88 deficiency severely impaired the response to malaria infection of CD27((-)), IL-17A-producing ?? T cells, but not of IFN-?-producing ?? cells. Instead, the latter compartment was severely contracted by ablating CD27, which synergizes with TCR?? in the induction of antiapoptotic mediators and cell cycle-promoting genes in CD27((+)), IFN-?-secreting ?? T cells. Hence, innate versus adaptive receptors differentially control the peripheral pool sizes of discrete proinflammatory ?? T cell subsets during immune responses to infection.

SUBMITTER: Ribot JC 

PROVIDER: S-EPMC3915338 | biostudies-literature | 2010 Dec

REPOSITORIES: biostudies-literature

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Cutting edge: adaptive versus innate receptor signals selectively control the pool sizes of murine IFN-γ- or IL-17-producing γδ T cells upon infection.

Ribot Julie C JC   Chaves-Ferreira Miguel M   d'Orey Francisco F   Wencker Mélanie M   Gonçalves-Sousa Natacha N   Decalf Jérémie J   Simas João P JP   Hayday Adrian C AC   Silva-Santos Bruno B  

Journal of immunology (Baltimore, Md. : 1950) 20101029 11


γδ T lymphocytes are commonly viewed as embracing properties of both adaptive and innate immunity. Contributing to this is their responsiveness to pathogen products, either with or without the involvement of the TCR and its coreceptors. This study clarifies this paradoxical behavior by showing that these two modes of responsiveness are the properties of two discrete sets of murine lymphoid γδ T cells. Thus, MyD88 deficiency severely impaired the response to malaria infection of CD27((-)), IL-17A  ...[more]

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