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Publication : 2B4 Is Dispensable for T-Dependent B Cell Immune Responses, but Its Deficiency Leads to Enhanced T-Independent Responses Due to an Increase in Peritoneal Cavity B1b Cells.

First Author  Ray A Year  2015
Journal  PLoS One Volume  10
Issue  8 Pages  e0137314
PubMed ID  26323020 Mgi Jnum  J:243014
Mgi Id  MGI:5907422 Doi  10.1371/journal.pone.0137314
Citation  Ray A, et al. (2015) 2B4 Is Dispensable for T-Dependent B Cell Immune Responses, but Its Deficiency Leads to Enhanced T-Independent Responses Due to an Increase in Peritoneal Cavity B1b Cells. PLoS One 10(8):e0137314
abstractText  The signaling lymphocyte activation molecule (SLAM) family plays important roles in adaptive immune responses. Herein, we evaluated whether the SLAM family member 2B4 (CD244) plays a role in immune cell development, homeostasis and antibody responses. We found that the splenic cellularity in Cd244-/- mice was significantly reduced due to a reduction in both CD4 T cells and follicular (Fo) B cells; whereas, the number of peritoneal cavity B cells was increased. These findings led us to examine whether 2B4 modulates B cell immune responses. When we examined T-dependent B cell responses, while there was no difference in the kinetics or magnitude of the antigen-specific IgM and IgG1 antibody response there was a reduction in bone marrow (BM) memory, but not plasma cells in Cd244-/- mice. When we evaluated T-independent immune responses, we found that antigen-specific IgM and IgG3 were elevated in the serum following immunization. These data indicate that 2B4 dampens T-independent B cell responses due to a reduction in peritoneal cavity B cells, but has minimal impact on T-dependent B cell responses.
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