Show simple item record

dc.contributor.authorJames, Kylie R
dc.contributor.authorSoon, Megan SF
dc.contributor.authorSebina, Ismail
dc.contributor.authorFernandez-Ruiz, Daniel
dc.contributor.authorDavey, Gayle
dc.contributor.authorLiligeto, Urijah N
dc.contributor.authorNair, Arya Sheela
dc.contributor.authorFogg, Lily G
dc.contributor.authorEdwards, Chelsea L
dc.contributor.authorBest, Shannon E
dc.contributor.authorLansink, Lianne IM
dc.contributor.authorSchroder, Kate
dc.contributor.authorWilson, Jane AC
dc.contributor.authorEngwerda, Christian R
dc.contributor.authoret al.
dc.date.accessioned2020-02-21T05:44:11Z
dc.date.available2020-02-21T05:44:11Z
dc.date.issued2018
dc.identifier.issn0022-1767en_US
dc.identifier.doi10.4049/jimmunol.1700782en_US
dc.identifier.urihttp://hdl.handle.net/10072/391788
dc.description.abstractDifferentiation of CD4+ Th cells is critical for immunity to malaria. Several innate immune signaling pathways have been implicated in the detection of blood-stage Plasmodium parasites, yet their influence over Th cell immunity remains unclear. In this study, we used Plasmodium-reactive TCR transgenic CD4+ T cells, termed PbTII cells, during nonlethal P. chabaudi chabaudi AS and P. yoelii 17XNL infection in mice, to examine Th cell development in vivo. We found no role for caspase1/11, stimulator of IFN genes, or mitochondrial antiviral-signaling protein, and only modest roles for MyD88 and TRIF-dependent signaling in controlling PbTII cell expansion. In contrast, IFN regulatory factor 3 (IRF3) was important for supporting PbTII expansion, promoting Th1 over T follicular helper (Tfh) differentiation, and controlling parasites during the first week of infection. IRF3 was not required for early priming by conventional dendritic cells, but was essential for promoting CXCL9 and MHC class II expression by inflammatory monocytes that supported PbTII responses in the spleen. Thereafter, IRF3-deficiency boosted Tfh responses, germinal center B cell and memory B cell development, parasite-specific Ab production, and resolution of infection. We also noted a B cell-intrinsic role for IRF3 in regulating humoral immune responses. Thus, we revealed roles for IRF3 in balancing Th1- and Tfh-dependent immunity during nonlethal infection with blood-stage Plasmodium parasites.en_US
dc.description.peerreviewedYesen_US
dc.languageEnglishen_US
dc.publisherAmerican Association of Immunologistsen_US
dc.relation.ispartofpagefrom1443en_US
dc.relation.ispartofpageto1456en_US
dc.relation.ispartofissue4en_US
dc.relation.ispartofjournalThe Journal of Immunologyen_US
dc.relation.ispartofvolume200en_US
dc.subject.fieldofresearchImmunologyen_US
dc.subject.fieldofresearchcode1107en_US
dc.subject.keywordsScience & Technologyen_US
dc.subject.keywordsLife Sciences & Biomedicineen_US
dc.subject.keywordsDENDRITIC CELLSen_US
dc.subject.keywordsB-CELLSen_US
dc.titleIFN Regulatory Factor 3 Balances Th1 and T Follicular Helper Immunity during Nonlethal Blood-Stage Plasmodium Infectionen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Articlesen_US
dcterms.bibliographicCitationJames, KR; Soon, MSF; Sebina, I; Fernandez-Ruiz, D; Davey, G; Liligeto, UN; Nair, AS; Fogg, LG; Edwards, CL; Best, SE; Lansink, LIM; Schroder, K; Wilson, JAC; Austin, R; Suhrbier, A; Lane, SW; Hill, GR; Engwerda, CR; Heath, WR; Haque, A, IFN Regulatory Factor 3 Balances Th1 and T Follicular Helper Immunity during Nonlethal Blood-Stage Plasmodium Infection,The Journal of Immunology, 2018, 200 (4), pp. 1443-1456en_US
dcterms.dateAccepted2017-12-12
dc.date.updated2020-02-21T05:41:51Z
gro.rights.copyrightSelf-archiving of the author-manuscript version is not yet supported by this journal. Please refer to the journal link for access to the definitive, published version or contact the author[s] for more information.en_US
gro.hasfulltextNo Full Text
gro.griffith.authorEngwerda, Christian R.


Files in this item

FilesSizeFormatView

There are no files associated with this item.

This item appears in the following Collection(s)

  • Journal articles
    Contains articles published by Griffith authors in scholarly journals.

Show simple item record