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The Interaction of Human Pathogenic Fungi With C-Type Lectin Receptors.
Front Immunol. 2018; 9:1261.FI

Abstract

Fungi, usually present as commensals, are a major cause of opportunistic infections in immunocompromised patients. Such infections, if not diagnosed or treated properly, can prove fatal. However, in most cases healthy individuals are able to avert the fungal attacks by mounting proper antifungal immune responses. Among the pattern recognition receptors (PRRs), C-type lectin receptors (CLRs) are the major players in antifungal immunity. CLRs can recognize carbohydrate ligands, such as β-glucans and mannans, which are mainly found on fungal cell surfaces. They induce proinflammatory immune reactions, including phagocytosis, oxidative burst, cytokine, and chemokine production from innate effector cells, as well as activation of adaptive immunity via Th17 responses. CLRs such as Dectin-1, Dectin-2, Mincle, mannose receptor (MR), and DC-SIGN can recognize many disease-causing fungi and also collaborate with each other as well as other PRRs in mounting a fungi-specific immune response. Mutations in these receptors affect the host response and have been linked to a higher risk in contracting fungal infections. This review focuses on how CLRs on various immune cells orchestrate the antifungal response and on the contribution of single nucleotide polymorphisms in these receptors toward the risk of developing such infections.

Authors+Show Affiliations

Institute for Microbiology and Hygiene, Charité - Universitätsmedizin Berlin, Berlin, Germany. Septomics Research Center, Jena University Hospital, Jena, Germany.Septomics Research Center, Jena University Hospital, Jena, Germany. International Leibniz Research School for Microbial and Biomolecular Interactions, Leibniz Institute for Natural Product Research and Infection Biology/Hans Knöll Institute, Jena, Germany.Septomics Research Center, Jena University Hospital, Jena, Germany.Septomics Research Center, Jena University Hospital, Jena, Germany.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

29915598

Citation

Goyal, Surabhi, et al. "The Interaction of Human Pathogenic Fungi With C-Type Lectin Receptors." Frontiers in Immunology, vol. 9, 2018, p. 1261.
Goyal S, Castrillón-Betancur JC, Klaile E, et al. The Interaction of Human Pathogenic Fungi With C-Type Lectin Receptors. Front Immunol. 2018;9:1261.
Goyal, S., Castrillón-Betancur, J. C., Klaile, E., & Slevogt, H. (2018). The Interaction of Human Pathogenic Fungi With C-Type Lectin Receptors. Frontiers in Immunology, 9, 1261. https://doi.org/10.3389/fimmu.2018.01261
Goyal S, et al. The Interaction of Human Pathogenic Fungi With C-Type Lectin Receptors. Front Immunol. 2018;9:1261. PubMed PMID: 29915598.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The Interaction of Human Pathogenic Fungi With C-Type Lectin Receptors. AU - Goyal,Surabhi, AU - Castrillón-Betancur,Juan Camilo, AU - Klaile,Esther, AU - Slevogt,Hortense, Y1 - 2018/06/04/ PY - 2018/03/09/received PY - 2018/05/18/accepted PY - 2018/6/20/entrez PY - 2018/6/20/pubmed PY - 2018/6/20/medline KW - Aspergillus KW - C-type lectin receptor KW - Candida KW - pathogenic fungi KW - pattern recognition receptor KW - single nucleotide polymorphisms SP - 1261 EP - 1261 JF - Frontiers in immunology JO - Front Immunol VL - 9 N2 - Fungi, usually present as commensals, are a major cause of opportunistic infections in immunocompromised patients. Such infections, if not diagnosed or treated properly, can prove fatal. However, in most cases healthy individuals are able to avert the fungal attacks by mounting proper antifungal immune responses. Among the pattern recognition receptors (PRRs), C-type lectin receptors (CLRs) are the major players in antifungal immunity. CLRs can recognize carbohydrate ligands, such as β-glucans and mannans, which are mainly found on fungal cell surfaces. They induce proinflammatory immune reactions, including phagocytosis, oxidative burst, cytokine, and chemokine production from innate effector cells, as well as activation of adaptive immunity via Th17 responses. CLRs such as Dectin-1, Dectin-2, Mincle, mannose receptor (MR), and DC-SIGN can recognize many disease-causing fungi and also collaborate with each other as well as other PRRs in mounting a fungi-specific immune response. Mutations in these receptors affect the host response and have been linked to a higher risk in contracting fungal infections. This review focuses on how CLRs on various immune cells orchestrate the antifungal response and on the contribution of single nucleotide polymorphisms in these receptors toward the risk of developing such infections. SN - 1664-3224 UR - https://www.unboundmedicine.com/medline/citation/29915598/The_Interaction_of_Human_Pathogenic_Fungi_With_C_Type_Lectin_Receptors_ DB - PRIME DP - Unbound Medicine ER -