Dectin-1 Stimulation Selectively Reinforces LPS-driven IgG1 Production by Mouse B Cells.
- Author:
Beom Seok SEO
1
;
Sang Hoon LEE
;
Ju Eon LEE
;
Yung Choon YOO
;
Junglim LEE
;
Seok Rae PARK
Author Information
- Publication Type:Brief Communication
- Keywords: Dectin-1; B cell; IgG1; C-type lectin receptor; Fungal immunity
- MeSH: Animals; Antibody Formation; B-Lymphocytes*; Candida albicans; Cell Proliferation; Cell Wall; Dendritic Cells; Immunoglobulin G*; Lectins, C-Type; Macrophages; Mice*; RNA, Messenger; Saccharomyces cerevisiae; Sprains and Strains; Zymosan
- From:Immune Network 2013;13(5):205-212
- CountryRepublic of Korea
- Language:English
- 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.
