Dectin-1 agonist selectively induces IgG1 class switching by LPS-activated mouse B cells
Beom-Seok Seo1, Ha-Yan Park1, Hee-Kyung Yoon1
1Department of Microbiology, Myunggok Medical Research Center, College of Medicine, Konyang University, Daejeon 35365, Republic of Korea.
Immunology Letters
|August 30, 2016
Summary
Heat-killed Saccharomyces cerevisiae selectively enhances IgG1 production by activating Dectin-1 on B cells. This promotes specific IgG1 class switching, leading to increased IgG1 antibody secretion.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Heat-killed Saccharomyces cerevisiae (HKSC) activates Dectin-1, a key receptor for fungal β-glucans.
- Previous studies showed HKSC enhances IgG1 production in LPS-stimulated mouse B cells.
Purpose of the Study:
- To investigate if HKSC-mediated IgG1 enhancement results from selective IgG1 class switching.
- To elucidate the role of Dectin-1 in this selective immune response.
Main Methods:
- RT-PCR to measure germline transcripts (GLTs).
- Flow cytometry to detect Ig-expressing B cells.
- ELISPOT assays to quantify Ig-secreting cells.
- Use of Dectin-1 antagonists (laminarin, antibody) and a selective agonist (depleted zymosan).
Main Results:
- HKSC selectively boosted GLTγ1 expression, IgG1+ B cells, and IgG1-secreting cells.
- HKSC induced CD69 (activation marker) and surface Dectin-1 expression.
- Dectin-1 antagonists inhibited HKSC-induced IgG1 production.
- Selective Dectin-1 agonist (dzn) also enhanced GLTγ1 and IgG1 production, blocked by antagonists.
Conclusions:
- Dectin-1 agonists directly stimulate Dectin-1 on LPS-activated B cells.
- This stimulation selectively induces IgG1 class switching.
- Results indicate a mechanism for selective IgG1 production via Dectin-1 signaling.
