RGD Reference Report - Th17 cells and IL-17 receptor signaling are essential for mucosal host defense against oral candidiasis. - Rat Genome Database

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Th17 cells and IL-17 receptor signaling are essential for mucosal host defense against oral candidiasis.

Authors: Conti, Heather R  Shen, Fang  Nayyar, Namrata  Stocum, Eileen  Sun, Jianing N  Lindemann, Matthew J  Ho, Allen W  Hai, Justine Hoda  Yu, Jeffrey J  Jung, Ji Won  Filler, Scott G  Masso-Welch, Patricia  Edgerton, Mira  Gaffen, Sarah L 
Citation: Conti HR, etal., J Exp Med. 2009 Feb 16;206(2):299-311. doi: 10.1084/jem.20081463. Epub 2009 Feb 9.
RGD ID: 39457957
Pubmed: PMID:19204111   (View Abstract at PubMed)
PMCID: PMC2646568   (View Article at PubMed Central)
DOI: DOI:10.1084/jem.20081463   (Journal Full-text)

The commensal fungus Candida albicans causes oropharyngeal candidiasis (OPC; thrush) in settings of immunodeficiency. Although disseminated, vaginal, and oral candidiasis are all caused by C. albicans species, host defense against C. albicans varies by anatomical location. T helper 1 (Th1) cells have long been implicated in defense against candidiasis, whereas the role of Th17 cells remains controversial. IL-17 mediates inflammatory pathology in a gastric model of mucosal candidiasis, but is host protective in disseminated disease. Here, we directly compared Th1 and Th17 function in a model of OPC. Th17-deficient (IL-23p19(-/-)) and IL-17R-deficient (IL-17RA(-/-)) mice experienced severe OPC, whereas Th1-deficient (IL-12p35(-/-)) mice showed low fungal burdens and no overt disease. Neutrophil recruitment was impaired in IL-23p19(-/-) and IL-17RA(-/-), but not IL-12(-/-), mice, and TCR-alphabeta cells were more important than TCR-gammadelta cells. Surprisingly, mice deficient in the Th17 cytokine IL-22 were only mildly susceptible to OPC, indicating that IL-17 rather than IL-22 is vital in defense against oral candidiasis. Gene profiling of oral mucosal tissue showed strong induction of Th17 signature genes, including CXC chemokines and beta defensin-3. Saliva from Th17-deficient, but not Th1-deficient, mice exhibited reduced candidacidal activity. Thus, the Th17 lineage, acting largely through IL-17, confers the dominant response to oral candidiasis through neutrophils and antimicrobial factors.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
IL23AHumanoral candidiasis severityISOIl23a (Mus musculus) RGD 
Il23aRatoral candidiasis severityISOIl23a (Mus musculus) RGD 
Il23aMouseoral candidiasis severityIMP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Il23a  (interleukin 23 subunit alpha)

Genes (Mus musculus)
Il23a  (interleukin 23, alpha subunit p19)

Genes (Homo sapiens)
IL23A  (interleukin 23 subunit alpha)


Additional Information