Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2015 Aug 1;195(3):780-8.
doi: 10.4049/jimmunol.1500909.

IL-17-Mediated Immunity to the Opportunistic Fungal Pathogen Candida albicans

Heather R Conti  1 , Sarah L Gaffen  2
Affiliations
Review

IL-17-Mediated Immunity to the Opportunistic Fungal Pathogen Candida albicans

Heather R Conti et al. J Immunol. .

Abstract

IL-17 (IL-17A) has emerged as a key mediator of protection against extracellular microbes, but this cytokine also drives pathology in various autoimmune diseases. Overwhelming data in both humans and mice reveal a clear and surprisingly specific role for IL-17 in protection against the fungus Candida albicans, a commensal microbe of the human oral cavity, gastrointestinal tract, and reproductive mucosa. The IL-17 pathway regulates antifungal immunity through upregulation of proinflammatory cytokines, including IL-6, neutrophil-recruiting chemokines (e.g., CXCL1 and CXCL5), and antimicrobial peptides (e.g., defensins), which act in concert to limit fungal overgrowth. This review focuses on diseases caused by C. albicans, the role of IL-17-mediated immunity in candidiasis, and the implications for clinical therapies for both autoimmune conditions and fungal infections.

PubMed Disclaimer

Figures

Figure 1
Figure 1. Adaptive and Innate Immune Responses to C. albicans
C. albicans exists in various morphologies, which are sensed by PRRs such as C-type lectin receptors found on APCs as well as epithelial cells. Exposure to C. albicans induces expression of innate cytokines, many of which are inductive for IL-17-expression cells. Various sources of IL-17 are documented in the context of candidiasis, including innate and adaptive cell types. IL-17 signaling on epithelial or other non-hematopoietic cells leads to expression of chemokines, AMPs and other factors that contribute to fungal control.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Romani L. Immunity to fungal infections. Nat Rev Immunol. 2011;11:275–288. - PubMed
    1. Dongari-Bagtoglou A, Fidel P. The host cytokine responses and protective immunity in oropharyngeal candidiasis. J Dent Res. 2005;84:966–977. - PubMed
    1. Brown GD, Denning DW, Gow NA, Levitz SM, Netea MG, White TC. Hidden killers: human fungal infections. Sci Transl Med. 2012;4:165rv113. - PubMed
    1. Merseguel KB, Nishikaku AS, Rodrigues AM, Padovan AC, RC EF, Salles de Azevedo Melo A, da Silva Briones MR, Colombo AL. Genetic diversity of medically important and emerging Candida species causing invasive infection. BMC Infect Dis. 2015;15:57. - PMC - PubMed
    1. Jacobsen ID, Wilson D, Wachtler B, Brunke S, Naglik JR, Hube B. Candida albicans dimorphism as a therapeutic target. Exp Rev Anti-Infect Ther. 2012;10:85–93. - PubMed

Publication types

MeSH terms