Th17 cells and IL-17 receptor signaling are essential for mucosal host defense against oral candidiasis Article (Web of Science)


  • 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-αβ cells were more important than TCR-γδ 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 β 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.


  • 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.

publication date

  • 2009

published in

number of pages

  • 12

start page

  • 299

end page

  • 311


  • 206


  • 2