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In Vitro Differentiation Model of Human Normal Memory B Cells to Long-lived Plasma Cells
Published on: January 20, 2019
Galectin-3 regulates peritoneal B1-cell differentiation into plasma cells.
Felipe L Oliveira1, Roger Chammas, Lauremília Ricon
1Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Glycobiology
|August 22, 2009
Summary
Galectin-3 deficiency alters B1 lymphocyte populations in mice, favoring B1b cells and promoting B1a cell differentiation into plasma cells. This impacts peritoneal cavity immune cell balance.
Area of Science:
- Immunology
- Cell Biology
Background:
- Extracellular galectin-3 regulates B2 lymphocyte functions.
- The role of galectin-3 in B1 lymphocyte physiology remains less understood.
Purpose of the Study:
- To investigate galectin-3's role in B1-cell physiology.
- To analyze the impact of galectin-3 on the balance between B1a and B1b lymphocytes in the peritoneal cavity.
Main Methods:
- Analysis of galectin-3 knockout (galectin-3(-/-)) mice and wild-type controls.
- Flow cytometry to assess lymphocyte populations and surface marker expression (B220, CD43).
- Microscopy to evaluate cell adhesion and location within the peritoneal cavity.
Main Results:
- Galectin-3(-/-) mice exhibited reduced B1a lymphocytes and increased B1b lymphocytes.
- B1a cell differentiation into plasma cells was associated with abnormal mesenteric adhesion in galectin-3(-/-) mice.
- B220 expression was upregulated, and CD43 was downregulated on B1 lymphocytes in galectin-3(-/-) mice.
Conclusions:
- Absence of galectin-3 favors B1-cell differentiation into plasma cells.
- Peritoneal B1-cell population equilibrium is maintained by a compensatory increase in B1b lymphocytes in galectin-3(-/-) mice.
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