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      The role of Syk/CARD9 coupled C-type lectins in antifungal immunity

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          Abstract

          Fungal infections are affecting an increasing number of people, and the failure of current therapies in treating systemic infection has resulted in an unacceptably high mortality rate. It is therefore of importance that we understand immune mechanisms operating during fungal infections, in order to facilitate development of adjunctive immunotherapies for the treatment of these diseases. C-type lectin receptors (CLRs) are pattern recognition receptors (PRRs) that are critical for immune responses to fungi. Many of these receptors are coupled to Syk kinase, which allows these receptors to signal via CARD9 leading to NF-κB activation, which in turn contributes to the induction of both innate and adaptive immunity. Dectin-1, Dectin-2 and Mincle are all CLRs that share this common signalling mechanism and have been shown to play key roles in antifungal immunity. This review aims to update existing paradigms and summarise the most recent findings on these CLRs, their signal transduction mechanisms and the collaborations between these CLRs and other PRRs.

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          Dectin-1 is required for beta-glucan recognition and control of fungal infection.

          Philip Taylor, S Tsoni, Janet Willment … (2007)
          Beta-glucan is one of the most abundant polysaccharides in fungal pathogens, yet its importance in antifungal immunity is unclear. Here we show that deficiency of dectin-1, the myeloid receptor for beta-glucan, rendered mice susceptible to infection with Candida albicans. Dectin-1-deficient leukocytes demonstrated significantly impaired responses to fungi even in the presence of opsonins. Impaired leukocyte responses were manifested in vivo by reduced inflammatory cell recruitment after fungal infection, resulting in substantially increased fungal burdens and enhanced fungal dissemination. Our results establish a fundamental function for beta-glucan recognition by dectin-1 in antifungal immunity and demonstrate a signaling non-Toll-like pattern-recognition receptor required for the induction of protective immune responses.
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            Th17 cells and IL-17 receptor signaling are essential for mucosal host defense against oral candidiasis

            Heather Conti, Fang-Fang Shen, Namrata Nayyar … (2009)
            The commensal fungus Candida albicans causes oropharyngeal candidiasis (OPC; thrush) in settings of immunodeficiency. Although disseminated, vaginal, and oral candidiasis are all caused by C. albicans species, host defense against C. albicans varies by anatomical location. T helper 1 (Th1) cells have long been implicated in defense against candidiasis, whereas the role of Th17 cells remains controversial. IL-17 mediates inflammatory pathology in a gastric model of mucosal candidiasis, but is host protective in disseminated disease. Here, we directly compared Th1 and Th17 function in a model of OPC. Th17-deficient (IL-23p19−/−) and IL-17R–deficient (IL-17RA−/−) mice experienced severe OPC, whereas Th1-deficient (IL-12p35−/−) mice showed low fungal burdens and no overt disease. Neutrophil recruitment was impaired in IL-23p19−/− and IL-17RA−/−, but not IL-12−/−, mice, and TCR-αβ cells were more important than TCR-γδ cells. Surprisingly, mice deficient in the Th17 cytokine IL-22 were only mildly susceptible to OPC, indicating that IL-17 rather than IL-22 is vital in defense against oral candidiasis. Gene profiling of oral mucosal tissue showed strong induction of Th17 signature genes, including CXC chemokines and β defensin-3. Saliva from Th17-deficient, but not Th1-deficient, mice exhibited reduced candidacidal activity. Thus, the Th17 lineage, acting largely through IL-17, confers the dominant response to oral candidiasis through neutrophils and antimicrobial factors.
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              Syk- and CARD9-dependent coupling of innate immunity to the induction of T helper cells that produce interleukin 17.

              Salomé Leibundgut-Landmann, Olaf Gross, Matthew J. Robinson … (2007)
              The C-type lectin dectin-1 binds to yeast and signals through the kinase Syk and the adaptor CARD9 to induce production of interleukin 10 (IL-10) and IL-2 in dendritic cells (DCs). However, whether this pathway promotes full DC activation remains unclear. Here we show that dectin-1-Syk-CARD9 signaling induced DC maturation and the secretion of proinflammatory cytokines, including IL-6, tumor necrosis factor and IL-23, but little IL-12. Dectin-1-activated DCs 'instructed' the differentiation of CD4+ IL-17-producing effector T cells (T(H)-17 cells) in vitro, and a dectin-1 agonist acted as an adjuvant promoting the differentiation of T(H)-17 and T helper type 1 cells in vivo. Infection with Candida albicans induced CARD9-dependent T(H)-17 responses to the organism. Our data indicate that signaling through Syk and CARD9 can couple innate to adaptive immunity independently of Toll-like receptor signals and that CARD9 is required for the development of T(H)-17 responses to some pathogens.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Eur J Immunol
                Journal ID (iso-abbrev): Eur. J. Immunol
                Journal ID (publisher-id): eji
                Title: European Journal of Immunology
                Publisher: WILEY-VCH Verlag (Weinheim )
                ISSN (Print): 0014-2980
                ISSN (Electronic): 1521-4141
                Publication date (Print): February 2011
                Publication date (Electronic): 10 December 2010
                Volume: 41
                Issue: 2
                Pages: 276-281
                Affiliations
                [1 ]simpleAberdeen Fungal Group, Section of Immunity and Infection, Institute of Medical Sciences, University of Aberdeen Aberdeen, Scotland, UK
                [2 ]simpleDivision of Molecular Immunology, Medical Mycology Research Centre, Chiba University 1-8-1 Inohana, Chuo-Ku, Chiba, Japan
                [3 ]simpleInstitute of Medical Sciences, Centre for Experimental Medicine and Systems Biology, University of Tokyo Minato Ku, Tokyo, Japan
                Author notes
                Full correspondence: Dr. Gordon D. Brown, University of Aberdeen, Aberdeen Fungal Group, Section of Immunity and Infection, Institute of Medical Sciences, Aberdeen, AB25 2ZD, Scotland e-mail: gordon.brown@ 123456abdn.ac.uk Fax: 44-1224-555 766
                [*]

                These authors contributed equally to the work.

                Article
                DOI: 10.1002/eji.201041252
                PMC ID: 3434674
                PubMed ID: 21267996
                SO-VID: aa56c2dd-f430-4ac1-81d7-d41d7414b14a
                Copyright © Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
                License:

                Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation.

                History
                Date received : 12 November 2010
                Date revision received : 02 December 2010
                Date accepted : 07 December 2010
                Categories
                Subject: Highlights

                ScienceOpen disciplines: Immunology
                Keywords: dectin-2,dectin-1,mincle,antifungal immunity
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: dectin-2, dectin-1, mincle, antifungal immunity

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