Abstract
The discovery of interleukin (IL)-17-mediated immunity has provided a robust framework upon which our current understanding of the mechanism involved in host defense against mucocutaneous candidiasis (CMC) has been built. Studies have shed light on how pattern recognition receptors expressed by innate immune cells recognize various components of Candida cell wall. Inborn errors of immunity affecting IL-17+ T cell differentiation have recently been defined, such as deficiencies of signal transducer and activator of transcription (STAT)3, STAT1, IL-12Rβ1 and IL-12p40, and caspase recruitment domain 9. Impaired receptor-ligand coupling was identified in patients with IL-17F and IL-17 receptor A (IL17RA) deficiency and autoimmune polyendocrine syndrome (APS) type 1. Mutation in the nuclear factor kappa B activator (ACT) 1 was described as a cause of impaired IL-17R-mediated signaling. CMC may be part of a complex clinical phenotype like in patients with deficiencies of STAT3, IL-12Rβ1/IL-12p40 and APS-1 or may be the only or dominant phenotypic manifestation of disease which is referred to as CMC disease. CMCD may result from deficiencies of STAT1, IL-17F, IL-17RA and ACT1. In this review we discuss how recent research on IL-17-mediated immunity shed light on host defense against mucocutaneous infection by Candida and howthe discovery of various germ-line mutations and the characterization of associated clinical phenotypes have provided insights into the role of CD4+IL-17+ lymphocytes in the regulation of anticandidal defense of body surfaces.
| Original language | English |
|---|---|
| Pages (from-to) | 348-363 |
| Number of pages | 16 |
| Journal | International Reviews of Immunology |
| Volume | 34 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - máj. 25 2015 |
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ASJC Scopus subject areas
- Immunology
- Immunology and Allergy
Cite this
The evolving view of IL-17-mediated immunity in defense against mucocutaneous candidiasis in humans. / Soltész, Beáta; Tóth, B.; Sarkadi, Adrien Katalin; Erdős, M.; Máródi, L.
In: International Reviews of Immunology, Vol. 34, No. 4, 25.05.2015, p. 348-363.Research output: Article
}
TY - JOUR
T1 - The evolving view of IL-17-mediated immunity in defense against mucocutaneous candidiasis in humans
AU - Soltész, Beáta
AU - Tóth, B.
AU - Sarkadi, Adrien Katalin
AU - Erdős, M.
AU - Máródi, L.
PY - 2015/5/25
Y1 - 2015/5/25
N2 - The discovery of interleukin (IL)-17-mediated immunity has provided a robust framework upon which our current understanding of the mechanism involved in host defense against mucocutaneous candidiasis (CMC) has been built. Studies have shed light on how pattern recognition receptors expressed by innate immune cells recognize various components of Candida cell wall. Inborn errors of immunity affecting IL-17+ T cell differentiation have recently been defined, such as deficiencies of signal transducer and activator of transcription (STAT)3, STAT1, IL-12Rβ1 and IL-12p40, and caspase recruitment domain 9. Impaired receptor-ligand coupling was identified in patients with IL-17F and IL-17 receptor A (IL17RA) deficiency and autoimmune polyendocrine syndrome (APS) type 1. Mutation in the nuclear factor kappa B activator (ACT) 1 was described as a cause of impaired IL-17R-mediated signaling. CMC may be part of a complex clinical phenotype like in patients with deficiencies of STAT3, IL-12Rβ1/IL-12p40 and APS-1 or may be the only or dominant phenotypic manifestation of disease which is referred to as CMC disease. CMCD may result from deficiencies of STAT1, IL-17F, IL-17RA and ACT1. In this review we discuss how recent research on IL-17-mediated immunity shed light on host defense against mucocutaneous infection by Candida and howthe discovery of various germ-line mutations and the characterization of associated clinical phenotypes have provided insights into the role of CD4+IL-17+ lymphocytes in the regulation of anticandidal defense of body surfaces.
AB - The discovery of interleukin (IL)-17-mediated immunity has provided a robust framework upon which our current understanding of the mechanism involved in host defense against mucocutaneous candidiasis (CMC) has been built. Studies have shed light on how pattern recognition receptors expressed by innate immune cells recognize various components of Candida cell wall. Inborn errors of immunity affecting IL-17+ T cell differentiation have recently been defined, such as deficiencies of signal transducer and activator of transcription (STAT)3, STAT1, IL-12Rβ1 and IL-12p40, and caspase recruitment domain 9. Impaired receptor-ligand coupling was identified in patients with IL-17F and IL-17 receptor A (IL17RA) deficiency and autoimmune polyendocrine syndrome (APS) type 1. Mutation in the nuclear factor kappa B activator (ACT) 1 was described as a cause of impaired IL-17R-mediated signaling. CMC may be part of a complex clinical phenotype like in patients with deficiencies of STAT3, IL-12Rβ1/IL-12p40 and APS-1 or may be the only or dominant phenotypic manifestation of disease which is referred to as CMC disease. CMCD may result from deficiencies of STAT1, IL-17F, IL-17RA and ACT1. In this review we discuss how recent research on IL-17-mediated immunity shed light on host defense against mucocutaneous infection by Candida and howthe discovery of various germ-line mutations and the characterization of associated clinical phenotypes have provided insights into the role of CD4+IL-17+ lymphocytes in the regulation of anticandidal defense of body surfaces.
KW - Candida
KW - Interleukin-17
KW - Interleukin-17 receptor-mediated signaling
KW - Mucocutaneous candidiasis disease
KW - Pattern-recognition receptors
KW - Signal transducer and activator of transcription
UR - http://www.scopus.com/inward/record.url?scp=84953887296&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84953887296&partnerID=8YFLogxK
U2 - 10.3109/08830185.2015.1049345
DO - 10.3109/08830185.2015.1049345
M3 - Article
C2 - 26154078
AN - SCOPUS:84953887296
VL - 34
SP - 348
EP - 363
JO - International Reviews of Immunology
JF - International Reviews of Immunology
SN - 0883-0185
IS - 4
ER -