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Immunity. 2015 Feb 17;42(2):356-366. doi: 10.1016/j.immuni.2015.01.008. Epub 2015 Feb 10.

Candida albicans morphology and dendritic cell subsets determine T helper cell differentiation.

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Department of Dermatology, Center for Immunology, University of Minnesota, Minneapolis, MN 55455, USA.
Department of Molecular and Cellular Biology, University of Minnesota, Minneapolis, MN 55455, USA.
Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
Aberdeen Fungal Group, Institute of Medical Sciences, University of Aberdeen, Aberdeen, AB25 2ZD, UK.
Baylor Institute for Immunology Research and INSERM U899 - ANRS Center for Human Vaccines, 3434 Live Oak Street, Dallas, TX 75204.
Department of Molecular Microbiology and Biotechnology, George Wise Faculty of Life Sciences Tel Aviv University, Ramat Aviv, 69978 Israel.
Contributed equally


Candida albicans is a dimorphic fungus responsible for chronic mucocutaneous and systemic infections. Mucocutaneous immunity to C. albicans requires T helper 17 (Th17) cell differentiation that is thought to depend on recognition of filamentous C. albicans. Systemic immunity is considered T cell independent. Using a murine skin infection model, we compared T helper cell responses to yeast and filamentous C. albicans. We found that only yeast induced Th17 cell responses through a mechanism that required Dectin-1-mediated expression of interleukin-6 (IL-6) by Langerhans cells. Filamentous forms induced Th1 without Th17 cell responses due to the absence of Dectin-1 ligation. Notably, Th17 cell responses provided protection against cutaneous infection while Th1 cell responses provided protection against systemic infection. Thus, C. albicans morphology drives distinct T helper cell responses that provide tissue-specific protection. These findings provide insight into compartmentalization of Th cell responses and C. albicans pathogenesis and have critical implications for vaccine strategies.

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