MyD88 Shapes Vaccine Immunity by Extrinsically Regulating Survival of CD4+ T Cells during the Contraction Phase

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dc.contributor.authorWang, Huafeng
dc.contributor.authorLi, Mengyi
dc.contributor.authorHung, Chiung-Yu
dc.contributor.authorSinha, Meenal
dc.contributor.authorLee, Linda M.
dc.contributor.authorWiesner, Darin L.
dc.contributor.authorLeBert, Vanessa
dc.contributor.authorLerksuthirat, Tassanee
dc.contributor.authorGalles, Kevin
dc.contributor.authorSuresh, Marulasiddappa
dc.contributor.authorDeFranco, Anthony L.
dc.contributor.authorLowell, Clifford A.
dc.contributor.authorKlein, Bruce S.
dc.contributor.authorWüthrich, Marcel
dc.date.accessioned2023-06-14T19:19:31Z
dc.date.available2023-06-14T19:19:31Z
dc.date.issued2016-08-19
dc.description.abstractSoaring rates of systemic fungal infections worldwide underscore the need for vaccine prevention. An understanding of the elements that promote vaccine immunity is essential. We previously reported that Th17 cells are required for vaccine immunity to the systemic dimorphic fungi of North America, and that Card9 and MyD88 signaling are required for the development of protective Th17 cells. Herein, we investigated where, when and how MyD88 regulates T cell development. We uncovered a novel mechanism in which MyD88 extrinsically regulates the survival of activated T cells during the contraction phase and in the absence of inflammation, but is dispensable for the expansion and differentiation of the cells. The poor survival of activated T cells in Myd88-/- mice is linked to increased caspase3-mediated apoptosis, but not to Fas- or Bim-dependent apoptotic pathways, nor to reduced expression of the anti-apoptotic molecules Bcl-2 or Bcl-xL. Moreover, TLR3, 7, and/or 9, but not TLR2 or 4, also were required extrinsically for MyD88-dependent Th17 cell responses and vaccine immunity. Similar MyD88 requirements governed the survival of virus primed T cells. Our data identify unappreciated new requirements for eliciting adaptive immunity and have implications for designing vaccines.en_US
dc.description.departmentMolecular Microbiology and Immunologyen_US
dc.description.sponsorshipNational Institutes of Healthen_US
dc.identifier.citationWang, H., Li, M., Hung, C. Y., Sinha, M., Lee, L. M., Wiesner, D. L., . . . Wüthrich, M. (2016). MyD88 Shapes Vaccine Immunity by Extrinsically Regulating Survival of CD4+ T Cells during the Contraction Phase. PLOS Pathogens, 12(8), e1005787. doi:10.1371/journal.ppat.1005787en_US
dc.identifier.issn1553-7374
dc.identifier.otherhttps://doi.org/10.1371/journal.ppat.1005787
dc.identifier.urihttps://hdl.handle.net/20.500.12588/1883
dc.language.isoen_USen_US
dc.publisherPublic Library of Scienceen_US
dc.rightsAttribution 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.titleMyD88 Shapes Vaccine Immunity by Extrinsically Regulating Survival of CD4+ T Cells during the Contraction Phaseen_US
dc.typeArticleen_US

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