The emerging fungal pathogen Candida auris induces IFNγ to colonize mammalian hair follicles
Open accessAbstract
Public health alarm concerning the emerging fungus Candida auris is fueled by its antifungal drug resistance and propensity to cause deadly outbreaks. Persistent skin colonization drives transmission and lethal sepsis although its basis remains mysterious. We compared the skin colonization dynamics of C. auris with its relative C. albicans , quantifying skin fungal persistence and distribution and immune composition and positioning. C. auris displayed a higher propensity to colonize hair follicles and avidly bound to human hair. While C. albicans triggered an effective sterilizing type 3/17 antifungal immune response driven by IL-17A/F-producing lymphocytes, C. auris triggered a type 1, IFNγ-driven immune response targeting hair follicles. Rather than promoting fungal clearance, IFNγ enhanced C. auris skin colonization by acting directly on keratinocytes impairing epithelial barrier integrity and repressing antifungal defense programs. C. auris exploits focal skin immune responses to create a niche for persistence in hair follicles.
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Written from the paper’s full text.
TL;DR
Candida auris persists on mouse skin by colonizing hair follicles and inducing a focal type 1, IFNγ-driven immune response that paradoxically supports fungal growth. IFNγ acts directly on upper hair follicle keratinocytes, suppressing antifungal and barrier programs, whereas C. albicans triggers sterilizing IL-17-dependent immunity.
Key findings
- After a single topical application, C. auris persisted throughout a 30-day time course, while C. albicans was undetectable by day 5; after four serial doses, C. albicans remained undetectable by 2 days after the final inoculum, whereas C. auris persisted in all animals.
- C. auris showed hair-binding activity and tropism to hair follicles: it colonized ~30% of hair follicles in undamaged skin, reduced to ~10% after depilatory cream pretreatment, compared with <5% for C. albicans.
- C. albicans induced >10-fold increases in Th17 cells and >3-fold increases in IL-17A production, whereas C. auris induced blunted Th17 responses and robust type 1 responses, including CD8+ Tc1, CD4+ Th1, IFNγ production, and cDC1 accumulation near the upper hair follicle.
- IFNγ promoted C. auris skin colonization: titers were reduced in IFNγ−/− mice and elevated in IFNγ-overexpressing mice; keratinocyte-specific IFNγR1 knockout reduced titers; IL-17−/− mice had ~10-fold higher titers after undamaged-skin rechallenge; IFNγ blockade reduced CFU in both WT and IL-17−/− mice.
Methods
- Mouse skin colonization models using C57BL/6 mice, shaved undamaged back or ear skin, topical C. auris or C. albicans, with CFU time courses, rechallenge, epicutaneous infection, and systemic infection; immune profiling by flow cytometry, scRNAseq, 3D confocal microscopy, and lineage tracing.
- Fungal strains included C. auris clade I–IV isolates NIH0388, NIH0381, NIH0383, NIH0385 and C. albicans SC5314; hair binding was tested in vitro with human hair fragments and calcofluor white staining.
- scRNAseq used 10x Genomics, CellRanger, Seurat clustering, and GSEA/ORA; imaging used Imaris for 3D quantification of immune cell positioning and keratinocyte Stat1/B2M expression.
Limitations
- The paper does not state a limitations section.
- Evident from the text: conclusions rely on mouse colonization models and in vitro human hair-binding assays; no human skin colonization or in vivo human infection data are presented.
- Evident from the text: scRNAseq experiment 2 used one replicate per group with pooled mice, and findings may vary by C. auris strain, body site, and skin damage status.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
3 of 4 cited sources checked · 0 supported · 0 flagged · accuracy not yet measured
- Findingown data
C. auris displays a unique ability to inhabit hair follicles.
“it displays unique abilities to bind hair, inhabit hair follicles, and induce highly focal IFNγ-dependent immune responses that reduce antifungal defenses and induce epithelial stress within keratinocytes of the upper hair follicle.”
Quote in the paperSubstantial claim - Findingown data
C. auris induces highly focal IFNγ-dependent immune responses.
“it displays unique abilities to bind hair, inhabit hair follicles, and induce highly focal IFNγ-dependent immune responses that reduce antifungal defenses and induce epithelial stress within keratinocytes of the upper hair follicle.”
Quote in the paperSubstantial claim - Findingown data
C. auris exhibits higher in vitro hair-binding activity than C. albicans.
“As predicted, C. auris exhibited higher in vitro hair-binding activity than C. albicans (Fig 1F; Fig1s1D,E).”
Quote in the paperSubstantial claim - Findingown data
C. auris displays a unique ability to bind hair.
“it displays unique abilities to bind hair, inhabit hair follicles, and induce highly focal IFNγ-dependent immune responses that reduce antifungal defenses and induce epithelial stress within keratinocytes of the upper hair follicle.”
Quote in the paperSubstantial claim - Findingown data
The IFNγ-dependent immune responses induced by C. auris reduce antifungal defenses.
“it displays unique abilities to bind hair, inhabit hair follicles, and induce highly focal IFNγ-dependent immune responses that reduce antifungal defenses and induce epithelial stress within keratinocytes of the upper hair follicle.”
Quote in the paperSubstantial claim
- Findingreasoning
The IFNγ-dependent immune responses induced by C. auris induce epithelial stress within keratinocytes of the upper hair follicle.
“it displays unique abilities to bind hair, inhabit hair follicles, and induce highly focal IFNγ-dependent immune responses that reduce antifungal defenses and induce epithelial stress within keratinocytes of the upper hair follicle.”
Quote in the paperSubstantial claim - Findingown data
C. auris but not C. albicans induces robust increases in type 1-polarized lymphocytes including Tc1, Th1, and their IFNγ production.
“Surprisingly, C. auris but not C. albicans induced robust increases in the abundance of type 1-polarized lymphocytes, including cytotoxic CD8+ Tc1 cells, helper CD4+ Th1, and their production of IFNγ (Fig 1J–K).”
Quote in the paperSubstantial claim - Findingreasoning
IFNγ signaling in keratinocytes enhances the ability of C. auris to colonize skin.
“and that IFNγ signaling in keratinocytes enhances the ability of C. auris to colonize skin.”
Quote in the paperSubstantial claim - Findingreasoning
C. auris is far less sensitive to IL-17-dependent restriction on skin than C. albicans.
“Our observations suggest C. auris is far less sensitive to IL-17-dependent restriction on skin than C. albicans.”
Quote in the paperSubstantial claim- Rests on an assumption: C. albicans is a highly adapted commensal of humans and other mammals that primarily inhabits the gut.
- Rests on an assumption: Invasion of C. albicans into deeper tissues is dramatically restricted by IL-17-dependent immunity.
- Findingreasoning
C. auris elicits a type 1 immune response in skin that is opposite to the response elicited by C. albicans and IL-17.
“opposite to the response elicited by C. albicans and IL-17—and that IFNγ signaling in keratinocytes enhances the ability of C. auris to colonize skin.”
Quote in the paperSubstantial claim - Findingreasoning
The interactions of C. auris and C. albicans with mammalian skin are strikingly different.
“Still, the interactions of C. auris and C. albicans with mammalian skin are strikingly different”
Quote in the paperSubstantial claim- Rests on an assumption: C. albicans is a highly adapted commensal of humans and other mammals that primarily inhabits the gut.
- Rests on an assumption: Invasion of C. albicans into deeper tissues is dramatically restricted by IL-17-dependent immunity.
- Interpretationown data
C. auris skin colonization is supported by induced IFNγ signaling that acts directly on skin keratinocytes.
“indicating that C. auris skin colonization is supported by induced IFNγ signaling that acts directly on skin keratinocytes.”
Quote in the paperSubstantial claim- Rests on an assumption: Mouse models of skin colonization reproduce key features of human C. auris skin colonization.
- Interpretationown data
C. auris skin colonization drives a type 1, IFNγ-associated immune response distinct from the response to C. albicans.
“Consistent with our flow cytometric results, the scRNAseq data suggest that C. auris skin colonization drives a type 1, IFNγ-associated immune response that is distinct from the response to C. albicans.”
Quote in the paperSubstantial claim- Rests on an assumption: Mouse models of skin colonization reproduce key features of human C. auris skin colonization.
- Interpretationown data
IFNγ paradoxically promotes the growth of C. auris on skin.
“suggesting that IFNγ paradoxically promotes the growth of C. auris on skin.”
Quote in the paperSubstantial claim- Rests on an assumption: Mouse models of skin colonization reproduce key features of human C. auris skin colonization.
- Interpretationown data
cDC1 cells are required for the expansion of Tc1 and Th1 cells in response to C. auris.
“We conclude that cDC1 cells, which are localized at the upper hair follicle near CD8+ cytotoxic T cells and CD4+ Th1 cells, are required for the expansion of Tc1 and Th1 cells in response to C. auris.”
Quote in the paperSubstantial claim - Interpretationown data
Direct binding to mammalian hair promotes localization of C. auris to hair follicles.
“These results indicate that direct binding to mammalian hair promotes the localization of C. auris to hair follicles.”
Quote in the paperSubstantial claim - Interpretationown data
IL-17 signaling through keratinocytes is required to restrict the growth of C. albicans on skin.
“Repetitive colonization of Ker14ΔIL17Ra mice phenocopied the colonized IL-17−/− animals (Fig 3A–B), indicating that IL-17 signaling through keratinocytes is required to restrict the growth of C. albicans on the skin.”
Quote in the paperSubstantial claim - Interpretationown data
IFNγ drives C. auris-associated responses in hair follicle keratinocytes.
“These results support a role for IFNγ in driving C. auris-associated responses in hair follicle keratinocytes.”
Quote in the paperSubstantial claim- Rests on an assumption: Mouse models of skin colonization reproduce key features of human C. auris skin colonization.
- Interpretationreasoning
C. auris enhances its own fitness in skin by inducing a localized type 1 immune response to create a hospitable niche for persistence within hair follicles.
“Based on these results, we propose that C. auris enhances its own fitness in skin by inducing a localized type 1 immune response to create a hospitable niche for persistence within hair follicles.”
Quote in the paperSubstantial claim
- Classified as probably not a substantial claim. 6
- May combine two claims. 5
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationType 3/17 immune responses characterized by IL-17A, IL-17F, and IL-22 are critical effectors of anti-fungal immunity.
“Based on studies of C. albicans, type 3/17 immune responses, characterized by the cytokines IL-17A, IL-17F, and IL-22, are thought to be the critical effectors of anti-fungal immunity14.”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [14] source
The Concluding remarks say IL-17-mediated defenses are essential against Candida albicans and probably other extracellular fungi. But “Antifungal cell-mediated immunity: Life after Th17” says IL-17F and IL-22 may participate in anti-Candida immunity and describes mixed findings for both. The source therefore does not establish all three cytokines as critical effectors of antifungal immunity generally. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationC. auris and C. albicans are related closely enough to share the same noncanonical genetic code.
“particularly for species related closely enough to share the same noncanonical genetic code40,41.”
Quote in the paperNot a substantial claim1 of 2 sources checked- cites [40] source
- cites [41] source
The Results (Functional annotation of C. auris; page not provided) place C. auris in the CUG clade based on codon-usage analysis. But the paper does not state that C. auris and C. albicans share the same noncanonical genetic code; its Discussion instead describes C. auris as highly divergent from C. albicans. (LLM, conf=0.81)
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationThere are currently no effective methods to eradicate C. auris from the skin.
“There are currently no effective methods to eradicate C. auris from the skin9.”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [9] source
The Discussion reports that patients remained colonized despite daily chlorhexidine washes, and the Conclusion says more information is needed on effective skin-decolonization regimens. These passages support the difficulty of clearing skin colonization, but they do not establish the categorical claim that no effective method exists. (LLM, conf=0.86)
Experimental — accuracy not yet measured
May combine two claims.
Findingown dataC. auris colonizes mouse skin with greater abundance and greater persistence than C. albicans.
“We conclude that C. auris colonizes mouse skin with greater abundance and greater persistence than C. albicans”
Quote in the paperSubstantial claimMay combine two claims.
FindingreasoningC. auris exhibits a remarkable facility for propagation and persistence on human skin.
“it exhibits a remarkable facility for propagation and persistence on human skin.”
Quote in the paperSubstantial claim- Rests on an assumption: C. auris is new to humans.
May combine two claims.
Findingown dataC. albicans stimulates a >10-fold increase in Th17 cells and a >3-fold increase in intracellular IL-17A production relative to mock.
“Relative to mock-colonized animals, C. albicans stimulated a >10-fold increase in the abundance of Th17 cells and a >3-fold increase in intracellular IL-17A production”
Quote in the paperNot a substantial claimMay combine two claims.
Interpretationown dataIL-17 signaling triggers sterilizing immune responses against C. albicans and, to some degree, C. auris, whereas IFNγ signaling selectively promotes the growth of C. auris in the skin.
“In aggregate, our findings suggest that IL-17 signaling triggers sterilizing immune responses against C. albicans and, to some degree, C. auris, whereas IFNγ signaling selectively promotes the growth of C. auris in the skin.”
Quote in the paperSubstantial claim- Rests on an assumption: Mouse models of skin colonization reproduce key features of human C. auris skin colonization.
Classified as probably not a substantial claim.
Study design and conductreasoningOlder mice were not used to ensure back skin hair follicles were harvested during the telogen hair follicle cycle.
“Older mice were not used to ensure back skin hair follicles were harvested during the telogen hair follicle cycle.”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationown dataC. albicans but not C. auris induces upper hair follicle keratinocytes to upregulate genetic programs that support epithelial barrier function.
“We were intrigued by the finding that C. albicans but not C. auris induces keratinocytes of the upper hair follicle—a region that functions as an organizational hub for skin immune cells28—to upregulate genetic programs that support epithelial barrier function.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S2 (checkable), S3 (load-bearing).
InterpretationreasoningThe multiplicity of mechanisms supporting the success of C. auris on the skin is suggestive of previous selection in a non-human mammalian host.
“Although the variables driving the recent emergence of C. auris into human populations remain mysterious, the multiplicity of mechanisms supporting the success of C. auris on the skin is suggestive of previous selection in a non-human mammalian host.”
Quote in the paperNot a substantial claim- Rests on an assumption: C. auris is new to humans.
Probably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone givenThe viable counts of the inocula were confirmed by plating serial dilutions on YPD agar plates.
“The viable counts of the inocula were confirmed by plating serial dilutions on YPD agar plates.”
Quote in the paperNot a substantial claim
The paper relies on this without support.
Mouse models of skin colonization reproduce key features of human C. auris skin colonization.
“we performed systematic comparisons of C. auris and C. albicans in mouse models of skin colonization”
The paper relies on this without support.
The fluorescent reporters and cell-surface markers used accurately identify the intended lymphocyte and APC populations.
“Type 1 and type 3/17 lymphocytes were visualized using mice that express fluorescently labeled reporters for the lymphocyte program-specific transcription factors, TbetZsGreen and RorγtGFP, respectively”
The paper relies on this without support.
The C. auris clinical isolates tested are representative of the species.
“we tested clinical isolates representing three other clades, as well as the original C. auris strain and C. albicans”
The paper relies on this without support.
C. albicans is a highly adapted commensal of humans and other mammals that primarily inhabits the gut.
“C. albicans is a highly adapted commensal of humans and other mammals that primarily inhabits the gut”
The paper relies on this without support.
Invasion of C. albicans into deeper tissues is dramatically restricted by IL-17-dependent immunity.
“invasion into deeper tissues is dramatically restricted by IL-17-dependent immunity.”
The paper relies on this without support.
C. auris is new to humans.
“although C. auris is new to humans”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Previous reports show C. auris residing on the skin surface and within hair follicles.
“This observation aligns with previous reports of C. auris residing on the skin surface and within hair follicles21,45.”
From Adhesin Als4112 promotes Candida auris skin colonization through interactions with keratinocytes and extracellular matrix proteins (2025) · cites this paper as [45]
Previous studies did not report skin invasion.
“However, skin invasion was not reported in previous studies21,45”
From Adhesin Als4112 promotes Candida auris skin colonization through interactions with keratinocytes and extracellular matrix proteins (2025) · cites this paper as [45]
The Main Text section on skin colonization reports this paper’s observation of C. auris in mouse hair follicles, but does not say whether earlier studies reported skin invasion. Searches for previous reports of invasion found discussion of prior skin-colonization research, not the claimed absence of invasion reports. (LLM, conf=0.72)
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Single-dose persistence time course extends beyond the stated harvest schedule
MinorThe results describe a 30-day time course after a single application, but the Methods list single-application CFU harvests only through day 12. The stated schedule does not account for the reported 30-day persistence.
“whereas C. auris persisted throughout the 30-day time course (Fig 1B).”
“Mice were colonized with a single application of yeast on day 0 then tissue was harvested for CFUs on days 2,5,8,10,12”
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Hurabielle, C., Link, V. M., Bouladoux, N., Han, S.-J., Merrill, E. D., Lightfoot, Y. L., Seto, N., Bleck, C. K. E., Smelkinson, M., Harrison, O. J., et al. (2020) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2003022117 · Cited by 97 · see citing works
Self-citationCandidiasis in Interferon- Knockout (IFN- -/-) Mice
Balish, E., Wagner, R. D., Vazquez-Torres, A., Pierson, C. L., & WARNER, T. F. C. S. (1998) · The Journal of Infectious Diseases · doi:10.1086/515645 · Cited by 96 · see citing works
The Role of Interferon-γ in Autoimmune Polyendocrine Syndrome Type 1
Oikonomou, V., Smith, G., Constantine, G. M., Schmitt, M. M., Ferré, E. M. N., Alejo, J. C., Riley, D., Kumar, D., Dias, L. D. S., Pechacek, J., et al. (2024) · New England Journal of Medicine · doi:10.1056/nejmoa2312665 · Cited by 89 · see citing works
IFN-gamma is required for IL-12 responsiveness in mice with Candida albicans infection.
Cenci, E., Mencacci, A., Sero, G. D., d’Ostiani, C. F., Mosci, P., Bacci, A., Montagnoli, C., Köpf, M., & Romani, L. R. (1998) · PubMed · Cited by 77 · see citing works
A Novel Model for IFN-γ–Mediated Autoinflammatory Syndromes
Reinhardt, R. L., Liang, H.-E., Bao, K., Price, A. E., Mohrs, M., Kelly, B. L., & Locksley, R. M. (2015) · The Journal of Immunology · doi:10.4049/jimmunol.1401992 · Cited by 74 · see citing works
Mantione, M. E., Meloni, M., Sana, I., Bordini, J., Del Nero, M., Riba, M., Ranghetti, P., Perotta, E., Ghia, P., Scarfò, L., et al. (2024) · Cell Death & Disease · doi:10.1038/s41419-024-06602-z · Cited by 57 · see citing works
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The broad impact of cell death genes on the human disease phenome
Rich, A., Lin, P., Gamazon, E. R., & Zinkel, S. S. (2024) · Cell Death and Disease · doi:10.1038/s41419-024-06632-7 · Cited by 6 · see citing works
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Sorted by citations
Zhao, G., Lyu, J., Veniaminova, N. A., Zarnowski, R., Mattos, E., Johnson, C. J., Quintanilla, D., Hautau, H., Hold, L. A., Xu, B., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-60876-1 · Cited by 32 · see citing works
“C. auris can reside on the skin and within murine hair follicles 21,45 .”
- Authors
- Merrill, E. D., Prudent, V., Moghadam, P., Rodriguez, A., Hurabielle, C., Wells, E. K. C., Basso, P., Scharschmidt, T. C., Rosenblum, M. D., Molofsky, A. B., & Noble, S. M.
- Affiliations
- University of California, San Francisco (US)
- Assistance Publique – Hôpitaux de Paris (FR)
- Corresponding author
- Noble, Suzanne M.
- ORCID
- Venue
- bioRxiv (Cold Spring Harbor Laboratory)
- Publisher
- openRxiv
- Published
- 2025-01-18
- PMC
- PMC11760791
- OpenAlex
- W4406575963
- Semantic Scholar
- 7a2eb5a111037308a3b8b42e0ef05dab038a9238
- Cited by
- 4
- References
- 42
- Citations by year
- 2026: 1 · 2025: 3
- Type
- posted content
- Language
- en
- Open access
- green
- doi.org
- Licence
- Locations
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (submittedVersion, cc-by-nc-nd)
- Funders
- National Institutes of Health (1r01ar084863-01, 5r21ai171789-02, 5t32ar007175-48, 5r01ai180438-02, 5t32ar079068-05)
- National Institute of Neurological Disorders and Stroke (R01NS126765)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Health Sciences › Medicine › Epidemiology › Nail Diseases and Treatments
- Health Sciences › Medicine › Epidemiology › Fungal Infections and Studies
- Keywords
- Candida auris, Candida albicans, skin colonization, hair follicle, interferon-gamma, type 1 immune response, IL-17A/F, keratinocytes, epithelial barrier integrity, antifungal immunity, fungal persistence, sepsis, antifungal resistance, fungal pathogenesis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-20.
Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-20.
Cited sources are checked by gpt-6-sol.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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