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Candida albicans-epithelial interactions and induction of mucosal innate immunity

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CURRENT OPINION IN MICROBIOLOGY
卷 40, 期 -, 页码 104-112

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CURRENT BIOLOGY LTD
DOI: 10.1016/j.mib.2017.10.030

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资金

  1. Medical Research Council [MR/M011372/1]
  2. Biotechnology & Biological Sciences Research Council [BB/N014677/1]
  3. National Institute for Health Research at Guys and St Thomas's NHS Foundation Trust
  4. King's College London Biomedical Research Centre [IS-BRC-1215-20006]
  5. Deutsche Forschungsgemeinschaft [SPP 1580 (Hu 528/17-1), CRC/TR124]
  6. German Federal Ministry of Education and Health [BMBF] [01EO1002]
  7. European Union's Horizon research and innovation programme under Marie Sklodowska-Curie Grant [642095]
  8. Leibniz Association InfectoOptics [SAS-2015-HKI-LWC]
  9. NIH [DE022550]
  10. Centre for Sepsis Control and Care (CSCC)
  11. BBSRC [BB/N014677/1] Funding Source: UKRI
  12. MRC [MR/M011372/1] Funding Source: UKRI
  13. Biotechnology and Biological Sciences Research Council [BB/N014677/1] Funding Source: researchfish
  14. Medical Research Council [MR/M011372/1] Funding Source: researchfish

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Candida albicans is a human fungal pathogen that causes millions of mucosal and life-threatening infections annually. C. albicans initially interacts with epithelial cells, resulting in fungal recognition and the formation of hyphae. Hypha formation is critical for host cell damage and immune activation, which are both driven by the secretion of Candidalysin, a recently discovered peptide toxin. Epithelial activation leads to the production of inflammatory mediators that recruit innate immune cells including neutrophils, macrophages and innate Type 17 cells, which together work with epithelial cells to clear the fungal infection. This review will focus on the recent discoveries that have advanced our understanding of C. albicans-epithelial interactions and the induction of mucosal innate immunity.

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