|
KMID : 0923620130130050205
|
|
Immune Network
2013 Volume.13 No. 5 p.205 ~ p.212
|
|
|
Dectin-1 Stimulation Selectively Reinforces LPS-driven IgG1 Production by Mouse B Cells
|
|
Seo Beom-Seok
Lee Sang-Hoon
Lee Ju-Eon
Yoo Yung-Choon
Lee Jung-Lim
Park Seok-Rae
|
|
|
Abstract
|
|
|
|
Dectin-1, which specifically recognizes ?-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, ?-glucan-stimulated Dectin-1 may cooperate with TLR4 to specifically enhance IgG1 production by mouse B cells.
|
|
|
KEYWORD
|
|
|
Dectin-1, B cell, IgG1, C-type lectin receptor, Fungal immunity
|
|
|
FullTexts / Linksout information
|
|
|
|
|
Listed journal information
|
|
   
|
|