Evolutionarily conserved recognition and innate immunity to fungal pathogens by the scavenger receptors SCARF1 and CD36

Means, Terry K.; Mylonakis, Eleftherios; Tampakakis, Emmanouil; Colvin, Richard A.; Seung, Edward; Puckett, Lindsay; Tai, Melissa; Stewart, Cameron R.; Pukkila-Worley, Read; Hickman, Suzanne E.; Moore, Kathryn J.; Calderwood, Stephen B.; Hacohen, Nir; Luster, Andrew D.; Khoury, Joseph El

doi:10.1084/jem.20082109

Cited by 218 publications

(189 citation statements)

References 62 publications

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“…abf-2 expression is regulated by the transcription factor HLH-30 following S. aureus infection [23]. Upregulation of abf-1 and abf-2 by infection with Cryptococcus neoformans requires the scavenger receptor CED-1 (homologous to human SCARF1) and C03F11.3 (homologous to human CD36) [76]. Moreover, expression of abf-1 was demonstrated to be dependent on the gene npr-1 in the context of P. aeruginosa infection [77].…”

Section: (F ) Defensin-like Antimicrobial Peptidesmentioning

confidence: 99%

Antimicrobial effectors in the nematode Caenorhabditis elegans : an outgroup to the Arthropoda

Dierking

Yang

Schulenburg

2016

Phil. Trans. R. Soc. B

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One contribution of 13 to a theme issue 'Evolutionary ecology of arthropod antimicrobial peptides'. Nematodes and arthropods likely form the taxon Ecdysozoa. Information on antimicrobial effectors from the model nematode Caenorhabditis elegans may thus shed light on the evolutionary origin of these defences in arthropods. This nematode species possesses an extensive armory of putative antimicrobial effector proteins, such as lysozymes, caenopores (or saposin-like proteins), defensin-like peptides, caenacins and neuropeptide-like proteins, in addition to the production of reactive oxygen species and autophagy. As C. elegans is a bacterivore that lives in microbe-rich environments, some of its effector peptides and proteins likely function in both digestion of bacterial food and pathogen elimination. In this review, we provide an overview of C. elegans immune effector proteins and mechanisms. We summarize the experimental evidence of their antimicrobial function and involvement in the response to pathogen infection. We further evaluate the microbe-induced expression of effector genes using WormExp, a recently established database for C. elegans gene expression analysis. We emphasize the need for further analysis at the protein level to demonstrate an antimicrobial activity of these molecules both in vitro and in vivo.This article is part of the themed issue 'Evolutionary ecology of arthropod antimicrobial peptides'.

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Section: (F ) Defensin-like Antimicrobial Peptidesmentioning

confidence: 99%

Antimicrobial effectors in the nematode Caenorhabditis elegans : an outgroup to the Arthropoda

Dierking

Yang

Schulenburg

2016

Phil. Trans. R. Soc. B

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“…121 CD36-deficient macrophages showed an »50% reduction in binding C. albicans relative to WT macrophage, 121 and CD36¡/¡ macrophages stimulated with C. albicans had a marked reduction in the expression of IL-1b, TNF, IL-12p40, MIP-2, MIP-1a, MIP-1b, and RANTES. 121 The chitin recognition receptors have also been investigated. On human peripheral blood mononuclear cells (PBMCs) and murine macrophages, purified chitin from C. albicans could block the recognition of C. albicans yeast cells.…”

Section: Prrs Of Neutrophils and Monocytes/macrophagesmentioning

confidence: 99%

“…Moreover, CD36 is a class B scavenger receptor that is a sensor for endogenous molecules and microbial products that signal via TLR2. 121 CHO-CD36 cells bind C. albicans also in a b-glucandependent manner. 121 CD36-deficient macrophages showed an »50% reduction in binding C. albicans relative to WT macrophage, 121 and CD36¡/¡ macrophages stimulated with C. albicans had a marked reduction in the expression of IL-1b, TNF, IL-12p40, MIP-2, MIP-1a, MIP-1b, and RANTES.…”

Section: Prrs Of Neutrophils and Monocytes/macrophagesmentioning

confidence: 99%

“…121 CHO-CD36 cells bind C. albicans also in a b-glucandependent manner. 121 CD36-deficient macrophages showed an »50% reduction in binding C. albicans relative to WT macrophage, 121 and CD36¡/¡ macrophages stimulated with C. albicans had a marked reduction in the expression of IL-1b, TNF, IL-12p40, MIP-2, MIP-1a, MIP-1b, and RANTES. 121 The chitin recognition receptors have also been investigated.…”

Section: Prrs Of Neutrophils and Monocytes/macrophagesmentioning

confidence: 99%

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The role of pattern recognition receptors in the innate recognition ofCandida albicans

Zheng

Wang

et al. 2015

Virulence

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“…The best-characterized fungal PAMP is b-glucan, which is absent in vertebrate tissues, but is the major component of the cell wall of most fungi [4]. Several PRRs, including dectin-1 [5] and scavenger receptors [6], are capable of binding b-glucan and triggering a diverse array of protective responses, including phagocytosis, the respiratory burst and the production of cytokines and chemokines [7]. In these activities, b-glucan receptors cooperate, to different extents, with Toll-like receptor 2 (TLR2) [8].…”

Section: Introductionmentioning

confidence: 99%

Recognition of yeast nucleic acids triggers a host‐protective type I interferon response

et al. 2011

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Although type I interferons (IFN-a/b) have been traditionally associated with antiviral responses, their importance in host defense against bacterial pathogens is being increasingly appreciated. Little is known, however, about the occurrence and functional role of IFN-a/b production in response to pathogenic yeasts. Here, we found that conventional DCs, but not macrophages nor plasmacytoid DCs, mounted IFN-b responses after in vitro stimulation with Candida spp. or Saccharomyces cerevisiae. These responses absolutely required MyD88, a Toll-like receptor (TLR) adaptor molecule, and were partially dependent on TLR9 and TLR7. Moreover, Candida DNA, as well as RNA, could recapitulate the IFN-b response. After intravenous challenge with Candida albicans, most mice lacking the IFN-a/b receptor died from their inability to control fungal growth, whereas all WT controls survived. These data suggest that recognition of yeast nucleic acids by TLR7 and TLR9 triggers a host-protective IFN-a/b response.Key words: Candida albicans . Cytokines . DCs . Fungal infections . Macrophages Supporting Information available online IntroductionCandida albicans (C. albicans) is, among fungi, the most common pathogen of humans. Although they are normally harmless commensals of the intestinal and urinary tract, C. albicans and other Candida species can cause recurrent mucosal infections in otherwise healthy subjects and life-threatening conditions in hospitalized or immunocompromised patients [1]. In recent years, C. albicans has become the fourth most common cause of bloodstream infections, with an incidence of between 1 and 24 cases per 100 000 and a mortality rate of 30-50% [2]. Since the host immune status is the major factor that determines the transition of C. albicans from commensalism to pathogenicity, elucidating the mechanisms underlying immune response initiation, particularly those underlying recognition of fungal components, is crucial to developing new and more effective strategies to combat these infections. In fact, despite the availability of new classes of antifungal drugs, current available therapies are only partially effective and are associated with significant side effects.Antimicrobial responses are initiated by the activation of germ-line-encoded receptors (pattern-recognition receptors, PRRs) expressed by cells of the innate immune system, mainly by macrophages and DCs, which monitor potential portals of pathogen entry. Each PRR binds directly or indirectly to one or more evolutionary conserved microbial molecules (pathogenassociated molecular patterns, PAMPs) and triggers intracellular signal transduction cascades culminating in distinctive transcriptional and nontranscriptional responses. By this mechanism, PRRs link microbial recognition with the selective activation of specific arms of the innate immune system [3].Ã These authors have contributed equally to this study. Eur. J. Immunol. 2011. 41: 1969-1979 DOI 10.1002 Immunity to infection 1969Considerable progress has been recently made in the identification ...

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Evolutionarily conserved recognition and innate immunity to fungal pathogens by the scavenger receptors SCARF1 and CD36

Cited by 218 publications

References 62 publications

Antimicrobial effectors in the nematode Caenorhabditis elegans : an outgroup to the Arthropoda

Antimicrobial effectors in the nematode Caenorhabditis elegans : an outgroup to the Arthropoda

The role of pattern recognition receptors in the innate recognition ofCandida albicans

Recognition of yeast nucleic acids triggers a host‐protective type I interferon response

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