Peer-reviewedCC BYImmunity
Antigen-restricted Candida albicans Th17 cells link oral-gut immunity and adopt pathogenic features during intestinal inflammation
13 affiliations
- 1Institute of Medical Immunology, Christian-Albrecht-University of Kiel, Kiel, Germany; Institute of Clinical Molecular Biology, Christian-Albrecht-University of Kiel, Kiel, Germany
- 2The Jill Roberts Institute for Research in Inflammatory Bowel Disease, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY 10021, USA
- 3Department of Internal Medicine I, University Medical Center Schleswig-Holstein Campus, Kiel, Kiel, Germany
- 4Institute of Clinical Molecular Biology, Christian-Albrecht-University of Kiel, Kiel, Germany; Department of Internal Medicine I, University Medical Center Schleswig-Holstein Campus, Kiel, Kiel, Germany
- 5Department of General, Visceral, Thoracic, Vascular and Transplantation Surgery, University Medical Center Rostock, Rostock, Germany
- 6Department of Dermatology and Allergy, University Hospital Schleswig-Holstein, Kiel, Germany
- 7Institute of Microbiology, Infectious Diseases and Immunology, Gastrointestinal Microbiology Research Group, Charité - University Medicine Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
- 8Clinic for Conservative Dentistry and Periodontology, University Hospital Schleswig-Holstein, Campus, Kiel, Kiel, Germany
- 9Department of Medicine, University of Wisconsin-Madison, Madison, WI, USA
- 10Department of Microbial Pathogenicity Mechanisms, Leibniz Institute for Natural Product Research and Infection Biology - Hans Knoell Institute (HKI), Jena, Germany
- 11Department of Microbial Pathogenicity Mechanisms, Leibniz Institute for Natural Product Research and Infection Biology - Hans Knoell Institute (HKI), Jena, Germany; Friedrich Schiller Universität Jena, Jena, Germany
- 12Department of Technical Immunology, Technische Universität Berlin, Berlin, Germany
- 13Institute of Medical Immunology, Christian-Albrecht-University of Kiel, Kiel, Germany; Institute of Clinical Molecular Biology, Christian-Albrecht-University of Kiel, Kiel, Germany. Electronic address: [email protected]
Abstract
The commensal yeast Candida albicans is a major inducer of human mucosal Th17 cells. How C. albicans drives Th17 cell responses at homeostasis, and whether such responses contribute to inflammatory diseases, remains poorly understood. Here, we showed that C. albicans-reactive Th17 cells targeted a limited set of proteins enriched in fungal extracellular vesicles. At homeostasis, these cells predominantly resided in the oral mucosa. However, T cell receptor profiling revealed shared clonotypes across oral and gut tissues, with C. albicans being a major driver of this repertoire overlap. In patients with Crohn's disease, C. albicans-specific Th17 cells with features of oral priming were enriched in intestinal tissues, where they retained their focused antigen specificity but acquired pathogenic Th17 cell traits. Together, our results reveal a stable, antigen-restricted C. albicans Th17 subset that is shared across mucosal sites and undergoes functional adaptation in the inflamed intestine. These cells represent a potential target for immune modulation in Crohn's disease.
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BibTeX
@article{martini2026antigenrestricted,
title = {{Antigen-restricted Candida albicans Th17 cells link oral-gut immunity and adopt pathogenic features during intestinal inflammation}},
author = {Gabriela Rios Martini and P. Hofmann and Ann-Kristin Kamps and Amos Weichberger and Ekaterina Tikhonova and Aidan Conroy and Xiangyu Pan and Diana Milagros Namuch and Laura Rathjens and Arne Bergfeld and Susanna Nikolaus and Jeanette Riffert and Florian Tran and Konrad Aden and Maria Witte and Clemens Schafmayer and Dora Stölzl and Stephan Weidinger and Markus M. Heimesaat and Miriam Cyris and Ann-Kristin Härdter and Christof Dörfer and Robert Żarnowski and David R. Andes and Sascha Brunke and Bernhard Hube and Alexander Scheffold and Iliyan Dimitrov Iliev and Stefan Schreiber and Petra Bächer},
journal = {Immunity},
year = {2026},
month = jul,
doi = {10.1016/j.immuni.2026.06.013},
url = {https://doi.org/10.1016/j.immuni.2026.06.013},
note = {CC BY},
}
RIS
TY - JOUR
TI - Antigen-restricted Candida albicans Th17 cells link oral-gut immunity and adopt pathogenic features during intestinal inflammation
AU - Gabriela Rios Martini
AU - P. Hofmann
AU - Ann-Kristin Kamps
AU - Amos Weichberger
AU - Ekaterina Tikhonova
AU - Aidan Conroy
AU - Xiangyu Pan
AU - Diana Milagros Namuch
AU - Laura Rathjens
AU - Arne Bergfeld
AU - Susanna Nikolaus
AU - Jeanette Riffert
AU - Florian Tran
AU - Konrad Aden
AU - Maria Witte
AU - Clemens Schafmayer
AU - Dora Stölzl
AU - Stephan Weidinger
AU - Markus M. Heimesaat
AU - Miriam Cyris
AU - Ann-Kristin Härdter
AU - Christof Dörfer
AU - Robert Żarnowski
AU - David R. Andes
AU - Sascha Brunke
AU - Bernhard Hube
AU - Alexander Scheffold
AU - Iliyan Dimitrov Iliev
AU - Stefan Schreiber
AU - Petra Bächer
PY - 2026
DA - 2026/07/14
JO - Immunity
DO - 10.1016/j.immuni.2026.06.013
UR - https://doi.org/10.1016/j.immuni.2026.06.013
AB - The commensal yeast Candida albicans is a major inducer of human mucosal Th17 cells. How C. albicans drives Th17 cell responses at homeostasis, and whether such responses contribute to inflammatory diseases, remains poorly understood. Here, we showed that C. albicans-reactive Th17 cells targeted a limited set of proteins enriched in fungal extracellular vesicles. At homeostasis, these cells predominantly resided in the oral mucosa. However, T cell receptor profiling revealed shared clonotypes across oral and gut tissues, with C. albicans being a major driver of this repertoire overlap. In patients with Crohn's disease, C. albicans-specific Th17 cells with features of oral priming were enriched in intestinal tissues, where they retained their focused antigen specificity but acquired pathogenic Th17 cell traits. Together, our results reveal a stable, antigen-restricted C. albicans Th17 subset that is shared across mucosal sites and undergoes functional adaptation in the inflamed intestine. These cells represent a potential target for immune modulation in Crohn's disease.
SN - 1074-7613
SN - 1097-4180
ER -