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Isolation and Th17 Differentiation of Na&#239;ve CD4 T Lymphocytes
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IL-17 and infections.

Y Ling1, A Puel2

  • 1Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM 1163, Paris, France; Imagine Institute, University Paris Descartes, Paris, France.

Actas Dermo-Sifiliograficas
|November 16, 2014
PubMed
Summary
This summary is machine-generated.

Interleukin-17 (IL-17) immunity is crucial for fighting Candida albicans infections. Deficiencies in IL-17 pathways lead to chronic mucocutaneous candidiasis (CMC) and increased susceptibility to other infections.

Keywords:
Candidiasis mucocutánea crónicaChronic mucocutaneous candidiasisErrores innatos de la inmunidad IL-17IL-17Inborn errors of IL-17 immunityInmunodeficiencias primariasPrimary immunodeficiencies

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Area of Science:

  • Immunology
  • Infectious Diseases
  • Genetics

Background:

  • Interleukin-17 (IL-17) mediated immunity is vital for host defense against fungal pathogens, particularly Candida albicans, at mucosal surfaces.
  • Defects in IL-17 immunity result in increased susceptibility to a wide range of infections beyond Candida.
  • Chronic mucocutaneous candidiasis (CMC) is a hallmark of genetic disorders affecting IL-17 pathways.

Purpose of the Study:

  • To elucidate the critical role of IL-17 immunity in mucocutaneous defense.
  • To highlight the spectrum of infections associated with IL-17 pathway deficiencies.
  • To underscore the significance of CMC as a clinical indicator of impaired IL-17 immunity.

Main Methods:

  • Review of clinical manifestations in patients with genetic defects affecting IL-17 immunity.
  • Analysis of immune responses in mouse models of IL-17 deficiency.
  • Correlation of specific genetic mutations (STAT3, STAT1, AIRE, IL-17F, IL-17RA, ACT1) with clinical phenotypes.

Main Results:

  • Patients with autosomal dominant (AD) hyper-IgE syndrome (HIES) and AD STAT1 gain-of-function mutations exhibit impaired IL-17 T-cell development and CMC.
  • Autosomal recessive (AR) autoimmune polyendocrine syndrome type 1 (APS-1) patients develop neutralizing autoantibodies against IL-17 cytokines, leading to CMC.
  • Inborn errors of IL-17 immunity, including AD IL-17F deficiency and AR IL-17RA or ACT1 deficiency, predominantly manifest as CMC.

Conclusions:

  • IL-17 immunity is indispensable for preventing Candida albicans infections of the skin, nails, and mucosae.
  • CMC serves as a primary clinical phenotype in various genetic disorders impacting IL-17 pathways.
  • Monitoring for CMC is essential in patients with IL-17 deficiencies and those undergoing anti-IL-17 therapies.