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Cited by 1Antifungal resistance and susceptibilityDermatology and Skin DiseasesT-cell and B-cell Immunology

Skin-resident T cells play an important role in controlling skin colonization of Candidozyma (Candida) auris

Open access
Xie, Jiajia, Yan, Liping, Kadosh, David, Xiong, Na·2026·iScience
DOI 10.1016/j.isci.2026.115862PMC PMC13194182
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Abstract

skin colonization.

AI snapshot

Written from the paper’s full text.

TL;DR

In mouse topical colonization models, skin-resident T cells, rather than infiltrating T cells, play the dominant role in controlling *Candidozyma (Candida) auris* skin colonization. CCR10-dependent skin-resident T cells and CD8+ skin-resident T cells are important, with both IL-17-dependent and IL-17-independent mechanisms implicated.

Key findings

  • FTY720 blockade of lymphocyte infiltration reduced skin γδT17 and CD8+ Tc17 cells but did not significantly change *C. auris* burdens after 1× or 2× topical application; after 2× applications, burdens were >20-fold lower than after 1×.
  • CCR10^EGFP/EGFP mice had increased *C. auris* skin colonization on day 6 after 1× application despite enhanced IL-17A+ CD8+ and CD4+ T cell responses and more severe skin inflammation; by day 13, *C. auris* levels were similarly low in CCR10^+/EGFP and CCR10^EGFP/EGFP mice.
  • Anti-IL-17A antibody treatment increased *C. auris* burdens in both CCR10^+/EGFP and CCR10^EGFP/EGFP mice, indicating IL-17A responses help compensate but are not sufficient.
  • FTY720-treated CD8-KO mice had significantly higher *C. auris* skin burdens than WT mice despite compensatory increases in CD4+ αβT cells, implicating skin-resident CD8+ T cells.

Methods

  • Mouse topical *C. auris* colonization: C57BL/6 WT, CCR10-KO/EGFP-KI, and CD8a-KO mice; shaved back skin; 1 × 10^9 *C. auris* cells (CDC #0383, African Clade) per application; 1×, 2×, or 4× every-other-day schemes; analysis on day 6 or 13.
  • Immune cells analyzed by flow cytometry after skin digestion and Percoll enrichment; fungal burden quantified by plating skin digests on CHROMagar Candida plates with PCR verification; FTY720 given at 1 mg/kg i.p. daily; anti-IL-17A given at 5 mg/kg before and 3 days after application.
  • Statistics: unpaired t test; data presented as mean ± SD; N = 5–10 depending on experiment.

Limitations

  • Stated: all experiments used a single *C. auris* strain (CDC #0383, African Clade), limiting extrapolation to other clades/strains; CCR10 may regulate non-T skin cells, so cell-specific CCR10-KO mice are needed; germline CD8a deletion may confound results, and inducible CD8+ T cell knockout would be more precise; other immune populations (DCs, macrophages, mast cells, neutrophils) were not addressed; findings need verification in human subsets.
  • Evident from the text: the study is mouse-only; IL-17-independent effector molecules remain unidentified; commensal bacteria were not experimentally controlled and may influence *C. auris* levels.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1016/j.isci.2026.115862

Cites

45 of 45 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

26 of 35 cited sources checked · 10 supported · 1 flagged · accuracy not yet measured

  • Premisecitation

    Homozygous CCR10-KO/EGFP-KI mice have dysregulated skin-resident T cells compared to heterozygous mice, characterized mostly by reduction of CD8+ and CD4+ αβT cells but not IL-17A+ αβT or γδT cells.

    “Homozygous CCR10-KO/EGFP-KI (CCR10EGFP/EGFP, or CCR10−/− for simplicity) mice have dysregulated skin-resident T cells compared to heterozygous CCR10-KO/EGFP-KI (CCR10+/EGFP or CCR10+/−) mice, characterized mostly by the reduction of CD8+ and CD4+ αβT cells but not IL-17A+ αβT or γδT cells.20,22,23”
    Quote in the paperSubstantial claim3 of 3 sources checked
    • cites [20] Xia, 2014, CCR10 regulates balanced maintenance and function of resident regulatory and effector T cells to promote immune homeostasis in the skin, J. Allergy Clin. Immunol. source

      The Results section on imbalanced maintenance reports fewer skin CD8+ and CD4+ αβT cells in CCR10−/− mice than in heterozygous controls. It also reports more γδT cells in the dermis, but does not establish that γδT cells are not reduced across the skin as a whole. The impaired immune homeostasis section reports a higher percentage of IL-17A+ CD4+ cells, not whether their absolute number is unchanged. (LLM, conf=0.84)

      Experimental — accuracy not yet measured
    • cites [22] Jin, 2010, CCR10 is important for the development of skin-specific gammadeltaT cells by regulating their migration and location, J. Immunol. source

      The Results sections on defective sIEL development and dermal accumulation report fewer epidermal Vγ3+ γδ T cells in CCR10-knockout mice and altered distribution of those cells within the skin—the opposite of the claim that γδ T cells were not reduced or dysregulated. The comparisons reported there are with wild-type controls, not heterozygous mice; these passages do not establish the claimed predominant loss of CD4+ and CD8+ αβ T cells. (LLM, conf=0.88)

      Checked by a reasoning model — may be wrong.

      Experimental — accuracy not yet measured
    • cites [23] Cai, 2014, Differential developmental requirement and peripheral regulation for dermal Vgamma4 and Vgamma6T17 cells in health and inflammation, Nat. Commun. source

      The Results section, ‘Thymic Vγ4 requires extrathymic environment for skin homing’ (page unavailable), reports that CCR10 deficiency did not reduce dermal Vγ4 cells relative to wild-type mice and that total dermal γδT-cell frequency was unchanged. The paper does not report the claimed reductions in CD8+ and CD4+ αβT cells or compare homozygous CCR10-KO/EGFP-KI mice with heterozygous mice. (LLM, conf=0.84)

      Experimental — accuracy not yet measured
  • Premisecitation

    IL-17-producing cells could exert effects in controlling C. auris colonization through IL-17-induced signals on skin keratinocytes to promote production of antimicrobial peptides.

    “IL-17-producing cells could exert their effects in controlling C. auris colonization through IL-17-induced signals on skin keratinocytes to promote the production of antimicrobial peptides (AMPs).6,16”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [6] Huang, 2021, Murine model of colonization with fungal pathogen Candida auris to explore skin tropism, host risk factors and therapeutic strategies, Cell Host Microbe source
    • cites [16] Lionakis, 2023, Immune responses to human fungal pathogens and therapeutic prospects, Nat. Rev. Immunol. source

      The Introduction reports that IL-17A and IL-17F from lymphocytes curtailed C. auris skin colonization in a mouse model. The Mucocutaneous candidiasis section says IL-17 signaling induces antimicrobial peptides in epithelial cells during mucosal Candida infection, but it does not establish that this mechanism operates through skin keratinocytes during C. auris colonization. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
  • Premisecitation

    Immune responses can control and eventually clear C. auris in immunocompetent hosts.

    “Immune responses can control and eventually clear C. auris in immunocompetent hosts.3,10”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [3] Lionakis, 2024, Candida auris Infections, N. Engl. J. Med. source
    • cites [10] Holt, 2024, Innate immune response to Candida auris, Curr. Opin. Microbiol. source

      The ‘Phagocyte responses to C. auris’ section says neutrophils help control infection in mice. It does not establish eventual clearance in immunocompetent hosts; the same section reports that C. auris can persist despite intact immunity. (LLM, conf=0.86)

      Experimental — accuracy not yet measured
  • Premisecitation

    C. auris induces weaker IL-17+ T cell responses than C. albicans does in an intradermal infection model of mice.

    “C. auris induces weaker IL-17+ T cell responses than C. albicans does in an intradermal infection model of mice,17 which might partially explain its prolonged skin colonization.”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [17] Datta, 2023, Differential skin immune responses in mice intradermally infected with Candida auris and Candida albicans, Microbiol. Spectr. source
  • Premisecitation

    Over-active IL-17A+ T cell responses also increase skin inflammation in CCR10EGFP/EGFP mice in an imiquimod-induced model of psoriasis.

    “Consistent with this finding, we previously found that over-active IL-17A+ T cell responses also increase skin inflammation in CCR10EGFP/EGFP mice in an imiquimod-induced model of psoriasis.44”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [44] Li, 2021, Psoriasis-associated impairment of CCL27/CCR10-derived regulation leads to IL-17A/IL-22-producing skin T-cell overactivation, J. Allergy Clin. Immunol. source
  • May combine two claims. 16
  • Classified as probably not a substantial claim. 15
  • The quote only partly states this claim. 1

  • May combine two claims.

    Premisecitation

    Coordinated activation of IL-17-producing γδT, αβT cells and ILCs in the skin controls C. auris colonization, while mice deficient in T cells and ILCs have an impaired ability to control and clear C. auris colonization.

    “Using a mouse model of topical C. auris application, Huang et al. first demonstrated that the coordinated activation of IL-17-producing γδT, αβT cells and innate lymphoid cells (ILCs) in the skin controls C. auris colonization, while mice deficient in T cells and ILCs have an impaired ability to control and clear C. auris colonization.6”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [6] Huang, 2021, Murine model of colonization with fungal pathogen Candida auris to explore skin tropism, host risk factors and therapeutic strategies, Cell Host Microbe source

  • Classified as probably not a substantial claim.

    Premisecitation

    IL-17+ T cell responses are important in controlling commensal fungi or fungal pathogens.

    “It was suggested that while IL-17+ T cell responses are important in controlling commensal fungi or fungal pathogens, they can promote tissue inflammatory diseases in predisposed hosts.41,42,43”
    Quote in the paperSubstantial claim1 of 3 sources checked
    • cites [41] Sparber, 2019, The Skin Commensal Yeast Malassezia Triggers a Type 17 Response that Coordinates Anti-fungal Immunity and Exacerbates Skin Inflammation, Cell Host Microbe source
    • cites [42] Ruchti, 2023, New insights into immunity to skin fungi shape our understanding of health and disease, Parasite Immunol. source
    • cites [43] Hurabielle, 2020, Immunity to commensal skin fungi promotes psoriasiform skin inflammation, Proc. Natl. Acad. Sci. USA source

  • May combine two claims.

    Premisecitation

    CCR10 is a chemokine receptor expressed by most skin-resident T cells and is critical for their homeostatic establishment through interaction with CCL27 expressed by keratinocytes.

    “CCR10 is a chemokine receptor expressed by most skin-resident T cells and is critical for their homeostatic establishment through interaction with its ligand CCL27, expressed by keratinocytes.20,21”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [20] Xia, 2014, CCR10 regulates balanced maintenance and function of resident regulatory and effector T cells to promote immune homeostasis in the skin, J. Allergy Clin. Immunol. source

      The Results report that a majority of skin-resident αβ T cells in mice express CCR10; the Discussion says CCR10 is critical for their migration into and balanced maintenance in skin under homeostatic conditions. The Introduction identifies CCL27 as its ligand, but our copy does not establish that interaction with keratinocyte-expressed CCL27 causes this effect. For healthy human skin, the Results report significant percentages of CCR10-positive T cells, not most skin-resident T cells. No page numbers are available in our copy. (LLM, conf=0.87)

      Experimental — accuracy not yet measured
    • cites [21] Davila, 2022, CCL27 is a crucial regulator of immune homeostasis of the skin and mucosal tissues, iScience source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    IL-23 produced by keratinocytes can activate skin-resident IL-17+ γδT cells to control bacterial and fungal pathogen infections.

    “it was previously reported that IL-23 produced by keratinocytes can activate skin-resident IL-17+ γδT cells to control bacterial and fungal pathogen infections.32,33”
    Quote in the paperNot a substantial claim2 of 2 sources checked
    • cites [32] Watson, 2024, The gene regulatory basis of bystander activation in CD8(+) T cells, Sci. Immunol. source

      The Discussion (page unavailable) says that subsets of neonatal γδ T cells secrete IL-17 upon activation, and reference 45 identifies a study in which IL-23 induces IL-17 production from γδ T cells. Our copy does not say that keratinocytes produce the IL-23, that the cells are skin-resident, or that this pathway controls bacterial and fungal infections. (LLM, conf=0.76)

      Experimental — accuracy not yet measured
    • cites [33] Cho, 2010, IL-17 is essential for host defense against cutaneous Staphylococcus aureus infection in mice, J. Clin. Investig. source

      The Results (page unavailable) show that IL-23 enhances IL-17 production by resident epidermal γδ T cells, and the Discussion (page unavailable) links these cells to defense against cutaneous S. aureus infection in mice. The paper does not establish that keratinocytes produce the IL-23 or that this pathway controls fungal infections. (LLM, conf=0.88)

      Experimental — accuracy not yet measured

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    IFNγ enhances re-infection of C. auris in an intradermal injection model of infection.

    “A recent report found that IFNγ enhances re-infection of C. auris in an intradermal injection model of infection.40”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [40] Das, 2025, The Emerging Fungal Pathogen Candida auris Induces IFNgamma to Colonize the Skin, PLoS Pathog. source

  • Classified as probably not a substantial claim.

    Premisecitation

    Topical C. auris application is considered more closely to mimic the natural process of skin colonization.

    “Topical C. auris application is considered more closely to mimic the natural process of skin colonization.6”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [6] Huang, 2021, Murine model of colonization with fungal pathogen Candida auris to explore skin tropism, host risk factors and therapeutic strategies, Cell Host Microbe source

  • May combine two claims.

    Premisecitation

    All skin-resident T cells are pre-activated T cells with effector/memory-like phenotypes, which could be activated in an innate fashion by alterations of molecular cues of the local tissue they reside in.

    “All skin-resident T cells are pre-activated T cells with effector/memory-like phenotypes, which could be activated in an innate fashion by alterations of molecular cues of the local tissue they reside in.26,27,28,29,30,31,32”
    Quote in the paperSubstantial claim5 of 7 sources checked
    • cites [26] Clark, 2010, Skin-resident T cells: the ups and downs of on site immunity, J. Invest. Dermatol. source

      In “Skin resident T cells: hiding in plain sight” (page unavailable), the review reports that over 95% of T cells in normal skin are memory T cells and 80% have an effector-memory phenotype; it does not say all are pre-activated. In “Local T cells responses in skin: lessons from psoriasis” (page unavailable), it describes activation of autoreactive T cells after local antigen-presenting cells produce IFNα. That example does not establish that all skin-resident T cells can be activated in an innate fashion by altered local molecular cues. (LLM, conf=0.88)

      Experimental — accuracy not yet measured
    • cites [27] Fu, 2016, Cutting Edge: Skin CCR10+ CD8+ T Cells Support Resident Regulatory T Cells through the B7.2/Receptor Axis To Regulate Local Immune Homeostasis and Response, J. Immunol. source

      The Results and Discussion section (page unavailable) reports that most EGFP+ OT-I CD8+ cells in skin after immunization had markers typical of resident memory T cells. This supports a memory-like phenotype for the studied cells, but not the claim that all skin-resident T cells are pre-activated. The paper also does not establish that local molecular cues activate them in an innate fashion; its described OT-I activation followed Ova immunization. (LLM, conf=0.86)

      Experimental — accuracy not yet measured
    • cites [28] Zareie, 2025, Cutaneous T cell immunity, Nat. Immunol. source
    • cites [29] Lauvau, 2016, Memory CD8(+) T Cells: Innate-Like Sensors and Orchestrators of Protection, Trends Immunol. source

      The Introduction identifies tissue-resident memory T cells as a memory CD8+ subset, and the ‘Sentinel cells’ section says inflammatory signals can reactivate memory CD8+ T cells without cognate antigen. But that section says circulating memory CD8+ cells mostly respond to those signals, while whether tissue-resident memory cells can respond to inflammatory cues alone remains unknown. The paper does not establish that all skin-resident T cells are pre-activated or have effector/memory-like phenotypes. Page numbers were not available in our copy. (LLM, conf=0.88)

      Experimental — accuracy not yet measured
    • cites [30] Lee, 2022, Significance of bystander T cell activation in microbial infection, Nat. Immunol. source
    • cites [31] Arkatkar, 2023, Memory T cells possess an innate-like function in local protection from mucosal infection, J. Clin. Investig. source

      The Results section on human mucosal tissue memory CD8+ T cells reports that local cytokines can trigger innate-like bystander activation. The paper does not establish that all skin-resident T cells are pre-activated or have effector/memory-like phenotypes; its findings concern memory CD8+ T cells, primarily in mucosal tissue. Page numbers are unavailable in our copy. (LLM, conf=0.88)

      Experimental — accuracy not yet measured
    • cites [32] Watson, 2024, The gene regulatory basis of bystander activation in CD8(+) T cells, Sci. Immunol. source

      The Introduction (page not provided) describes neonatal CD8+ T cells as effector-like before stimulation and able to respond to innate cytokines; it also describes inflammation-dependent, TCR-independent activation in a subset of naïve CD8+ T cells. The paper does not establish that all skin-resident T cells are pre-activated or that changes in local skin-tissue cues activate them. (LLM, conf=0.88)

      Experimental — accuracy not yet measured

  • Classified as probably not a substantial claim.

    Premisecitation

    IL-17+ T cell responses can promote tissue inflammatory diseases in predisposed hosts.

    “It was suggested that while IL-17+ T cell responses are important in controlling commensal fungi or fungal pathogens, they can promote tissue inflammatory diseases in predisposed hosts.41,42,43”
    Quote in the paperSubstantial claim1 of 3 sources checked
    • cites [41] Sparber, 2019, The Skin Commensal Yeast Malassezia Triggers a Type 17 Response that Coordinates Anti-fungal Immunity and Exacerbates Skin Inflammation, Cell Host Microbe source
    • cites [42] Ruchti, 2023, New insights into immunity to skin fungi shape our understanding of health and disease, Parasite Immunol. source
    • cites [43] Hurabielle, 2020, Immunity to commensal skin fungi promotes psoriasiform skin inflammation, Proc. Natl. Acad. Sci. USA source

  • The quote only partly states this claim.

    Findingown data

    Percentages of IL-17A+ γδT cells remained similar at early and late time points after 1× vs 2× C. auris applications.

    “while percentages of IL-17A+ γδT cells remained similar at the early and late time points (Figures 1C and 1D)”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Most skin IL-17A+ CD8+, CD4+ T cells and ILCs did not express CCR10(EGFP), while half of skin γδT17 cells were CCR10(EGFP)+ in CCR10+/EGFP mice.

    “On the other hand, most skin IL-17A+ CD8+, CD4+ T cells and ILCs did not express CCR10(EGFP), while half of skin γδT17 cells were CCR10(EGFP)+ in CCR10+/EGFP mice (Figure 3C).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    There was a relatively increased percentage of IFNγ+ γδT cells in FTY720-treated mice, although they represented a minor fraction of total γδT cells.

    “There was a relatively increased percentage of IFNγ+ γδT cells in FTY720-treated mice, although they represented a minor fraction of total γδT cells (Figure 2D).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    The percentage of CD3medium+ γδT cells was significantly reduced while percentages of CD4+ αβT cells increased in anti-IL-17A antibody-treated mice.

    “As a result, the percentage of CD3medium+ γδT cells, which include most γδT17 cells, was significantly reduced while percentages of CD4+ αβT cells increased in anti-IL-17A antibody-treated mice (Figure 4D).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    CCR10EGFP/EGFP littermates had significantly increased percentages of IL-17A+ CD8+ and CD4+ skin T cells, while they had similar percentages of IL-17A+ γδT cells and ILCs compared to CCR10+/EGFP mice.

    “Compared to CCR10+/EGFP mice, CCR10EGFP/EGFP littermates had significantly increased percentages of IL-17A+ CD8+ and CD4+ skin T cells, while they had similar percentages of IL-17A+ γδT cells and ILCs (Figures 3C and 3D).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    There were no significant differences in total and IFNγ+ ILCs, while IL-17A+ ILCs were increased in FTY720-treated mice compared to PBS-treated controls 6 days after 2× applications.

    “There were also no significant differences in total and IFNγ+ ILCs, while IL-17A+ ILCs were increased in FTY720-treated mice compared to PBS-treated controls (Figures 2F–2H).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    CCR10EGFP/EGFP and CCR10+/EGFP mice had similarly low levels of C. auris in the skin on day 13, both being greatly reduced from levels on day 6.

    “CCR10EGFP/EGFP and CCR10+/EGFP mice had similarly low levels of C. auris in the skin on day 13 (Figure S2E), both being greatly reduced from levels on day 6 (Figure 3E).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    CD8-KO mice had compensatorily increased percentages of CD4+ αβT cells, while they had similar γδT cells and ILCs in the skin on day 6 after 1× C. auris application compared to WT mice.

    “Compared to WT mice, CD8-KO mice had compensatorily increased percentages of CD4+ αβT cells, while they had similar γδT cells and ILCs in the skin on day 6 after 1× C. auris application (Figure 5A).”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Interpretationreasoning

    Commensal bacteria likely also have a role in the regulation of C. auris colonization.

    “Considering commensal bacteria play an important role in shaping skin-resident T cell repertoire, they likely also have a role in the regulation of C. auris colonization.”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: Commensal bacteria play an important role in shaping skin-resident T cell repertoire.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Interpretationcitation

    Different mechanisms for keratinocytes to sense C. auris colonization.

    “suggesting different mechanisms for keratinocytes to sense C. auris colonization.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationown data

    Both IL-17-dependent and independent responses of skin-resident T cells are required to control C. auris colonization and maintain skin tissue homeostasis, while imbalanced T cell responses led to impaired control of C. auris and increased skin inflammation in CCR10-KO mice.

    “We also found that both IL-17-dependent and independent responses of skin-resident T cells are required to control C. auris colonization and maintain skin tissue homeostasis, while imbalanced T cell responses led to impaired control of C. auris and increased skin inflammation in CCR10-KO mice.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationown data

    Blockage of infiltrating T cells by FTY720 does not significantly affect C. auris colonization suggests that innate-like responses of skin-resident T cells, but not adaptive responses of infiltrating T cells, play a major role in controlling C. auris colonization.

    “Our finding that blockage of infiltrating T cells by FTY720 does not significantly affect C. auris colonization suggests that innate-like responses of skin-resident T cells, but not adaptive responses of infiltrating T cells, play a major role in controlling C. auris colonization.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationown data

    A significant percentage of IL-17A+ γδT and αβT cells migrate into the skin in response to C. auris colonization, which is blocked by FTY720 treatment.

    “These results indicate that a significant percentage of IL-17A+ γδT and αβT cells migrate into the skin in response to the C. auris colonization, which is blocked by the FTY720 treatment.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    The current study used a single C. auris strain (CDC #0383, African Clade) in all experiments.

    “The current study used a single C. auris strain (CDC #0383, African Clade) in all experiments.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Card9 promotes IL-17+ T cell responses to some fungal pathogens.

    “The C-type lectin receptor adaptor molecule Card9 was found to promote IL-17+ T cell responses to some fungal pathogens”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationreasoning

    Imbalanced T cell responses in CCR10-KO mice lead to impaired control of pathogen infections and dysregulated skin immune homeostasis.

    “These results indicate that imbalanced T cell responses in CCR10-KO mice lead to impaired control of pathogen infections and dysregulated skin immune homeostasis.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationown data

    Increased IL-17A-producing T cells in CCR10EGFP/EGFP mice help to control C. auris colonization but are not sufficient to completely compensate for defective responses of CCR10-dependent skin-resident T cells.

    “These results support the notion that increased IL-17A-producing T cells in CCR10EGFP/EGFP mice help to control C. auris colonization but they are not sufficient to completely compensate for defective responses of CCR10-dependent skin-resident T cells.”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim.

    Study design and conductnone given

    The studies in this report focused on skin-resident cells.

    “Our studies in this report focused on skin-resident cells.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    Sex- and age-matched male and female mice were used.

    “Sex- and age-matched male and female mice were used.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    Littermates were used when possible.

    “Littermates were used when possible.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    All mice were on the C57BL/6 genetic background.

    “All mice were on the C57BL/6 genetic background and were raised in the SPF conditions.”
    Quote in the paperNot a substantial claim

  • Classified as probably not a substantial claim. May combine two claims.

    Study design and conductown data

    C. auris colonies were counted and their identities were verified using PCR.

    “Numbers of C. auris colonies were counted and their identities were verified using PCR.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    All mice were raised in SPF conditions.

    “All mice were on the C57BL/6 genetic background and were raised in the SPF conditions.”
    Quote in the paperNot a substantial claim
31 of 31

  • The paper relies on this without support.

    FTY720 treatment blocks T cell infiltration into the skin without affecting the function of skin-resident T cells.

    “Therefore, only responses of skin-resident T cells and ILCs would be involved in controlling C. auris skin colonization in FTY720-treated mice.”

  • The paper relies on this without support.

    CCR10 deficiency specifically impairs skin-resident T cell establishment without other confounding effects on antifungal immunity.

    “Homozygous CCR10-KO/EGFP-KI (CCR10EGFP/EGFP, or CCR10−/− for simplicity) mice have dysregulated skin-resident T cells compared to heterozygous CCR10-KO/EGFP-KI (CCR10+/EGFP or CCR10+/−) mice, characterized mostly by the reduction of CD8+ and CD4+ αβT cells but not IL-17A+ αβT or γδT cells.20,22,23”

  • The paper relies on this without support.

    CD8+ T cell deficiency specifically removes CD8+ T cells without other confounding effects that increase C. auris colonization.

    “we tested whether they played an important role in controlling C. auris skin colonization using CD8a-knockout (CD8-KO) mice, which are deficient of CD8+ T cells.24”

  • The paper relies on this without support.

    Commensal bacteria play an important role in shaping skin-resident T cell repertoire.

    “Considering commensal bacteria play an important role in shaping skin-resident T cell repertoire, they likely also have a role in the regulation of C. auris colonization.”

  • The paper relies on this without support.

    There is known genetic and phenotypic diversity among different clades of C. auris.

    “Given the known genetic and phenotypic diversity among different clades of C. auris, there is a limitation in extrapolating our findings to all other clades and strains.”
5 of 5

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Authors
Xie, J., Yan, L., Kadosh, D., & Xiong, N.
Affiliations
  • University of Science and Technology of China (CN)
  • The University of Texas at San Antonio Health Science Center (US)
Corresponding author
Xiong, Na
ORCID
Venue
iScience
Publisher
Elsevier BV
Published
2026-06
Volume
29
Issue
6
Pages
115862
ISSN
2589-0042 (ISSN-L)
DOI
10.1016/j.isci.2026.115862
PMC
PMC13194182
OpenAlex
W7155491874
Cited by
1
References
45
Citations by year
2026: 1
FWCI
4.94
Type
journal article
Language
en
Open access
Licence
Locations
  • iScience (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • PubMed Central (publishedVersion, cc-by)
Funders
  • National Cancer Institute (P30 CA054174)
  • National Center for Advancing Translational Sciences (UL1 TR002645)
  • University of Texas Health Science Center at Houston
  • National Institutes of Health
Topics
  • Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
  • Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords
skin-resident T cells, Candida auris, skin colonization, fungal skin infection, antifungal immunity, skin microbiome

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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