Evolutionarily conserved recognition and innate immunity to fungal pathogens by the scavenger receptors SCARF1 and CD36. J Exp Med 2009 Mar 16;206(3):637-53
Date
02/25/2009Pubmed ID
19237602Pubmed Central ID
PMC2699123DOI
10.1084/jem.20082109Scopus ID
2-s2.0-63449138494 (requires institutional sign-in at Scopus site) 195 CitationsAbstract
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 beta-glucan dependent. Thus, CED-1/SCARF1 and C03F11.3/CD36 are beta-glucan binding receptors and define an evolutionarily conserved pathway for the innate sensing of fungal pathogens.
Author List
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, El Khoury JAuthor
Lindsay L. Puckett MD Assistant Professor in the Radiation Oncology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsCD36 Antigens
Caenorhabditis elegans
Caenorhabditis elegans Proteins
Candida albicans
Candidiasis
Cell Adhesion
Conserved Sequence
Cryptococcosis
Cryptococcus neoformans
Cytokines
Evolution, Molecular
Immunity, Innate
Macrophage Activation
Macrophages
Membrane Proteins
Mice
RNA, Small Interfering
Receptors, Scavenger
Survival Analysis
Toll-Like Receptor 2