Found: 9
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Combinatorial actions of IL-22 and IL-17 drive optimal immunity to oral candidiasis through SPRRs.
- Published in:
- PLoS Pathogens, 2024, v. 0, n. 7, p. 1, doi. 10.1371/journal.ppat.1012302
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- Article
The Candida albicans toxin candidalysin mediates distinct epithelial inflammatory responses through p38 and EGFR-ERK pathways.
- Published in:
- Science Signaling, 2022, v. 15, n. 728, p. 1, doi. 10.1126/scisignal.abj6915
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- Article
The m<sup>6</sup>A reader IMP2 directs autoimmune inflammation through an IL-17– and TNFα-dependent C/EBP transcription factor axis.
- Published in:
- Science Immunology, 2021, v. 6, n. 61, p. 1, doi. 10.1126/sciimmunol.abd1287
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- Article
Restoring glucose uptake rescues neutrophil dysfunction and protects against systemic fungal infection in mouse models of kidney disease.
- Published in:
- Science Translational Medicine, 2020, v. 12, n. 548, p. 1, doi. 10.1126/scitranslmed.aay5691
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- Article
Oral epithelial IL-22/STAT3 signaling licenses IL-17–mediated immunity to oral mucosal candidiasis.
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- Science Immunology, 2020, v. 5, n. 48, p. 1, doi. 10.1126/sciimmunol.aba0570
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- Article
The Interleukin (IL) 17R/IL-22R Signaling Axis Is Dispensable for Vulvovaginal Candidiasis Regardless of Estrogen Status.
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- Journal of Infectious Diseases, 2020, v. 221, n. 9, p. 1554, doi. 10.1093/infdis/jiz649
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- Article
IL-17 Receptor Signaling Negatively Regulates the Development of Tubulointerstitial Fibrosis in the Kidney.
- Published in:
- Mediators of Inflammation, 2018, p. 1, doi. 10.1155/2018/5103672
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- Article
Oral epithelial cells orchestrate innate type 17 responses to Candida albicans through the virulence factor candidalysin.
- Published in:
- Science Immunology, 2017, v. 2, n. 17, p. 1, doi. 10.1126/sciimmunol.aam8834
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- Article
Signaling through IL-17C/IL-17RE Is Dispensable for Immunity to Systemic, Oral and Cutaneous Candidiasis.
- Published in:
- PLoS ONE, 2015, v. 10, n. 4, p. 1, doi. 10.1371/journal.pone.0122807
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- Article