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Molecular mechanisms of mucocutaneous immunity against Candida and Staphylococcus species

期刊

JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
卷 130, 期 5, 页码 1019-1027

出版社

MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2012.09.011

关键词

Primary immunodeficiency diseases; signal transducer and activator of transcription; signal transducer and activator of transcription 1 and 3; IL-17; Candida species; Staphylococcus species

资金

  1. Axa Fellowship
  2. National Center for Research Resources
  3. National Center for Advancing Sciences (National Institutes of Health)
  4. St Giles Foundation
  5. Pfizer
  6. GlaxoSmithKline
  7. NovImmune
  8. Merck
  9. Sanofi
  10. TAMOP [4.2.1./B-09/1/KONV-2010-0007]
  11. National Center for Research Resources [8UL1TR000043]
  12. National Center for Advancing Sciences (NCATS), National Institutes of Health
  13. ANR [GENCMCD 11-BSV3-005-01]
  14. AXA Research Fund

向作者/读者索取更多资源

Signal transducer and activator of transcription (STAT) proteins are key components of the innate and adaptive immune responses to pathogenic microorganisms. Recent research on primary immunodeficiency disorders and the identification of patients carrying germline mutations in STAT1, STAT3, and STAT5B have highlighted the role of human STATs in host defense against various viruses, bacteria, and fungi. Mutations in STAT1 and STAT3 disrupt various cytokine pathways that control mucocutaneous immunity against Candida species, especially Candida albicans, and Staphylococcus species, especially Staphylococcus aureus. Here we consider inborn errors of immunity arising from mutations in either STAT1 or STAT3 that affect mucocutaneous immunity to Candida and Staphylococcus species. (J Allergy Clin Immunol 2012;130:1019-27.)

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