The immune recognition of polysaccharide antigens is vital in both host defense against pathogens and general housekeeping functions in the body. CD36 is a Type-BI scavenger receptor expressed by multiple cell types including APCs and subsets of B cells. CD36 recognizes various endogenous and pathogen-derived ligands, including β-glucans, lipoteichoic acid, and oxidized phospholipids. Therefore, we hypothesized that CD36 would have important roles in the recognition of and host defense against pathogens bearing these ligands. We observed that mice lacking CD36 show increased susceptibility to infection by S. pyogenes and A. fumigatus, which express these ligands and had a decreased ability to generate anti-N-acetyl-D-glucosamine (GlcNAc) antibodies in response to immunization with S. pyogenes. CD36-/- APCs also exhibit a reduced capacity to phagocytose these microorganisms in vitro and in vivo. Additionally, we observed that mice lacking CD36 have an exacerbation of A. fumagatus-induced allergic airway disease and an accumulation of proinflammatory cells in the alveolar spaces of the lung. We propose that this is due to the reduced ability to clear A. fumigatus conidia and the diminished capacity of CD36-/- phagocytes to clear apoptotic cells. Our data suggest that CD36 on both B cells and APCs plays important roles in the development of anti-GlcNAc antibody responses and the clearance of allergens to modulate the development of allergic airway disease in mice.
- Copyright © 2013 by The American Association of Immunologists, Inc.