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Dectin-1 Stimulation Selectively Reinforces LPS-driven IgG1 Production by Mouse B Cells

  • Seo, Beom-Seok (Department of Microbiology, Myunggok Medical Research Institute, College of Medicine, Konyang University) ;
  • Lee, Sang-Hoon (Department of Microbiology, Myunggok Medical Research Institute, College of Medicine, Konyang University) ;
  • Lee, Ju-Eon (Department of Microbiology, Myunggok Medical Research Institute, College of Medicine, Konyang University) ;
  • Yoo, Yung-Choon (Department of Microbiology, Myunggok Medical Research Institute, College of Medicine, Konyang University) ;
  • Lee, Junglim (Department of Microbiology, Myunggok Medical Research Institute, College of Medicine, Konyang University) ;
  • Park, Seok-Rae (Department of Microbiology, Myunggok Medical Research Institute, College of Medicine, Konyang University)
  • Received : 2013.09.12
  • Accepted : 2013.09.24
  • Published : 2013.10.31

Abstract

Dectin-1, which specifically recognizes ${\beta}$-glucan of fungal cell walls, is a non-Toll-like receptor (TLR) pattern recognition receptor and a representative of C-type lectin receptors (CLRs). The importance of Dectin-1 in innate immune cells, such as dendritic cells and macrophages, has previously been well studied. However, the function of Dectin-1 in B cells is very poorly understood. To determine the role of Dectin-1 in B cell activation, we first investigated whether mouse B cells express Dectin-1 and then assessed the effect of Dectin-1 stimulation on B cell proliferation and antibody production. Mouse B cells express mRNAs encoding CLRs, including Dectin-1, and surface Dectin-1 was expressed in B cells of C57BL/6 rather than BALB/c strain. Dectin-1 agonists, heat-killed Candida albicans (HKCA) and heat-killed Saccharomyces cerevisiae (HKSC), alone induced B cell proliferation but not antibody production. Interestingly, HKSC, HKCA, and depleted zymosan (a selective Dectin-1 agonist) selectively enhanced LPS-driven IgG1 production. Taken together, these results suggest that, during fungal infection, ${\beta}$-glucan-stimulated Dectin-1 may cooperate with TLR4 to specifically enhance IgG1 production by mouse B cells.

Keywords

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