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The Emerging Fungal Pathogen Candida auris Induces IFNγ to Colonize the Skin
Diprasom Das1, Shrihari M Ganesh1, Abtar Mishra1
1Department of Comparative Pathobiology, College of Veterinary Medicine, Purdue University, West Lafayette, Indiana, United States of America.
Plos Pathogens
|April 28, 2025
Summary
Candida auris, a drug-resistant fungus, persists in skin by inducing harmful Th1 cells. This differs from Candida albicans and involves IFNγ, potentially offering new treatment targets.
Area of Science:
- Mycology
- Immunology
- Infectious Diseases
Background:
- Candida auris is a multidrug-resistant fungal pathogen causing severe human infections.
- Factors regulating C. auris skin infection remain poorly understood.
Purpose of the Study:
- To elucidate the immune response to C. auris skin infection.
- To understand the mechanisms behind C. auris skin persistence.
Main Methods:
- Comparative analysis of immune cell responses (Th1, Th17) to C. auris and Candida albicans.
- Investigation of the role of Interferon-gamma (IFNγ) in C. auris skin infection.
- Analysis of cytokine production (IL-12) and immune cell differentiation.
- Examination of the C. auris cell wall's role in immune modulation.
Main Results:
- C. auris predominantly induces pathogenic Th1 cells secreting IFNγ during reinfection, unlike protective Th17 cells induced by C. albicans.
- IFNγ was found to enhance C. auris skin infection by suppressing IL-17 responses and increasing dermal damage.
- IL-12, produced by inflammatory macrophages and dendritic cells, drives Th1 cell development.
- The C. auris outer mannan layer influences Th1 and Th17 cell development.
Conclusions:
- C. auris induces IFNγ to facilitate its persistence in the skin.
- This IFNγ-mediated mechanism explains the preferential long-term skin colonization of C. auris over C. albicans.
- Findings offer potential targets for novel therapeutic strategies against C. auris infections.
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