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

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

doi:10.1084/jem.20082109

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

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

Research output: Contribution to journal › Article › peer-review

210 Scopus citations

Abstract

Receptors involved in innate immunity to fungal pathogens have not been fully elucidated. We show that the Caenorhabditis elegans receptors CED-1 and C03F11.3, and their mammalian orthologues, the scavenger receptors SCARF1 and CD36, mediate host defense against two prototypic fungal pathogens, Cryptococcus neoformans and Candida albicans. CED-1 and C03F11.1 mediated antimicrobial peptide production and were necessary for nematode survival after C. neoformans infection. SCARF1 and CD36 mediated cytokine production and were required for macrophage binding to C. neoformans, and control of the infection in mice. Binding of these pathogens to SCARF1 and CD36 was β-glucan dependent. Thus, CED-1/SCARF1 and C03F11.3/CD36 are β-glucan binding receptors and define an evolutionarily conserved pathway for the innate sensing of fungal pathogens.

Original language	English (US)
Pages (from-to)	637-653
Number of pages	17
Journal	Journal of Experimental Medicine
Volume	206
Issue number	3
DOIs	https://doi.org/10.1084/jem.20082109
State	Published - Mar 16 2009

ASJC Scopus subject areas

Immunology and Allergy
Immunology

Divisions

Infectious Disease

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Means, T. K., Mylonakis, E., Tampakakis, E., Colvin, R. A., Seung, E., Puckett, L., Tai, M. F., Stewart, C. R., Pukkila-Worley, R., Hickman, S. E., Moore, K. J., Calderwood, S. B., Hacohen, N., Luster, A. D., & Khoury, J. E. (2009). Evolutionarily conserved recognition and innate immunity to fungal pathogens by the scavenger receptors SCARF1 and CD36. Journal of Experimental Medicine, 206(3), 637-653. https://doi.org/10.1084/jem.20082109

Means, TK, Mylonakis, E, Tampakakis, E, Colvin, RA, Seung, E, Puckett, L, Tai, MF, Stewart, CR, Pukkila-Worley, R, Hickman, SE, Moore, KJ, Calderwood, SB, Hacohen, N, Luster, AD & Khoury, JE 2009, 'Evolutionarily conserved recognition and innate immunity to fungal pathogens by the scavenger receptors SCARF1 and CD36', Journal of Experimental Medicine, vol. 206, no. 3, pp. 637-653. https://doi.org/10.1084/jem.20082109

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title = "Evolutionarily conserved recognition and innate immunity to fungal pathogens by the scavenger receptors SCARF1 and CD36",

abstract = "Receptors involved in innate immunity to fungal pathogens have not been fully elucidated. We show that the Caenorhabditis elegans receptors CED-1 and C03F11.3, and their mammalian orthologues, the scavenger receptors SCARF1 and CD36, mediate host defense against two prototypic fungal pathogens, Cryptococcus neoformans and Candida albicans. CED-1 and C03F11.1 mediated antimicrobial peptide production and were necessary for nematode survival after C. neoformans infection. SCARF1 and CD36 mediated cytokine production and were required for macrophage binding to C. neoformans, and control of the infection in mice. Binding of these pathogens to SCARF1 and CD36 was β-glucan dependent. Thus, CED-1/SCARF1 and C03F11.3/CD36 are β-glucan binding receptors and define an evolutionarily conserved pathway for the innate sensing of fungal pathogens.",

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AU - Colvin, Richard A.

AU - Seung, Edward

AU - Puckett, Lindsay

AU - Tai, Melissa F.

AU - Stewart, Cameron R.

AU - Pukkila-Worley, Read

AU - Hickman, Suzanne E.

AU - Moore, Kathryn J.

AU - Calderwood, Stephen B.

AU - Hacohen, Nir

AU - Luster, Andrew D.

AU - Khoury, Joseph El

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AB - Receptors involved in innate immunity to fungal pathogens have not been fully elucidated. We show that the Caenorhabditis elegans receptors CED-1 and C03F11.3, and their mammalian orthologues, the scavenger receptors SCARF1 and CD36, mediate host defense against two prototypic fungal pathogens, Cryptococcus neoformans and Candida albicans. CED-1 and C03F11.1 mediated antimicrobial peptide production and were necessary for nematode survival after C. neoformans infection. SCARF1 and CD36 mediated cytokine production and were required for macrophage binding to C. neoformans, and control of the infection in mice. Binding of these pathogens to SCARF1 and CD36 was β-glucan dependent. Thus, CED-1/SCARF1 and C03F11.3/CD36 are β-glucan binding receptors and define an evolutionarily conserved pathway for the innate sensing of fungal pathogens.

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

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