Authors

Rebecca A. Drummond, National Institutes of Health
Jigar V. Desai, National Institutes of Health
Amy P. Hsu, National Institutes of Health
Vasileios Oikonomou, National Institutes of Health
Donald C. Vinh, McGill University Health Centre
Joshua A. Acklin, Icahn School of Medicine at Mount Sinai
Michael S. Abers, National Institutes of Health
Magdalena A. Walkiewicz, National Institutes of Health
Sarah L. Anzick, National Institutes of Health
Muthulekha Swamydas, National Institutes of Health
Simon Vautier, National Institutes of Health
Mukil Natarajan, National Institutes of Health
Andrew J. Oler, National Institutes of Health
Daisuke Yamanaka, Tokyo University of Pharmacy and Life Sciences
Katrin D. Mayer-Barber, National Institutes of Health
Yoichiro Iwakura, Tokyo University of Science
David Bianchi, National Institutes of Health
Brian Driscoll, National Institutes of Health
Ken Hauck, National Institutes of Health
Ahnika Kline, National Institutes of Health
Nicholas S.P. Viall, National Institutes of Health
Christa S. Zerbe, National Institutes of Health
Elise M.N. Ferré, National Institutes of Health
Monica M. Schmitt, National Institutes of Health
Tom DiMaggio, National Institutes of Health
Stefania Pittaluga, National Cancer Institute
John A. Butman, National Institutes of Health
Adrian M. Zelazny, National Institutes of Health
Yvonne R. Shea, National Institutes of Health
Cesar A. Arias, Houston Methodist Hospital
Cameron Ashbaugh, University of California, San Francisco
Maryam Mahmood, Mayo Clinic
Zelalem Temesgen, Mayo Clinic
Alexander G. Theofiles, Mayo Clinic
Masayuki Nigo, University of Texas Health Science Center at Houston
Varsha Moudgal, St. Joseph Mercy Hospital
Karen C. Bloch, Vanderbilt University Medical Center
Sean G. Kelly, Vanderbilt University Medical Center
M. Suzanne Whitworth, Cook Children’s Health Care System
Ganesh Rao, Baylor College of Medicine
Cindy J. Whitener, Penn State Milton S. Hershey Medical Center
Neema Mafi, Mayo Clinic Hospital
Juan Gea-Banacloche, National Institutes of Health
Lawrence C. Kenyon, Thomas Jefferson UniversityFollow
William R. Miller, Houston Methodist Hospital
Katia Boggian, Cantonal Hospital St. Gallen
Andrea Gilbert, University of Texas Health, San Antonio
Matthew Sincock, National Institutes of Health
Alexandra F. Freeman, National Institutes of Health
John E. Bennett, Wilmington Health
Rodrigo Hasbun, University of Texas Health Science Center at Houston
Constantinos M. Mikelis, Texas Tech University Health Sciences Center
Kyung J. Kwon-Chung, National Institutes of Health
Yasmine Belkaid, National Institutes of Health
Gordon D. Brown, University of Exeter
Jean K. Lim, Icahn School of Medicine at Mount Sinai
Douglas B. Kuhns, Frederick National Laboratory for Cancer Research
Steven M. Holland, National Institutes of Health
Michail S. Lionakis, National Institutes of Health

Document Type

Article

Publication Date

11-15-2022

Comments

This is the author's final published version in the Journal of Clinical Investigation, Volume 132, Issue 22, November 2022, Article number e159348.

The published version is available at https://doi.org/10.1172/JCI159348.

Copyright © 2022, Drummond et al.

Abstract

Subcutaneous phaeohyphomycosis typically affects immunocompetent individuals following traumatic inoculation. Severe or disseminated infection can occur in CARD9 deficiency or after transplantation, but the mechanisms protecting against phaeohyphomycosis remain unclear. We evaluated a patient with progressive, refractory Corynespora cassiicola phaeohyphomycosis and found that he carried biallelic deleterious mutations in CLEC7A encoding the CARD9-coupled, β-glucan-binding receptor, Dectin-1. The patient's PBMCs failed to produce TNF-α and IL-1β in response to β-glucan and/or C. cassiicola. To confirm the cellular and molecular requirements for immunity against C. cassiicola, we developed a mouse model of this infection. Mouse macrophages required Dectin-1 and CARD9 for IL-1β and TNF-α production, which enhanced fungal killing in an interdependent manner. Deficiency of either Dectin-1 or CARD9 was associated with more severe fungal disease, recapitulating the human observation. Because these data implicated impaired Dectin-1 responses in susceptibility to phaeohyphomycosis, we evaluated 17 additional unrelated patients with severe forms of the infection. We found that 12 out of 17 carried deleterious CLEC7A mutations associated with an altered Dectin-1 extracellular C-terminal domain and impaired Dectin-1-dependent cytokine production. Thus, we show that Dectin-1 and CARD9 promote protective TNF-α- and IL-1β-mediated macrophage defense against C. cassiicola. More broadly, we demonstrate that human Dectin-1 deficiency may contribute to susceptibility to severe phaeohyphomycosis by certain dematiaceous fungi.

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.

PubMed ID

36377664

Language

English

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