title: 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.
abstract: 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.
authors: Blood Research Institute, BloodCenter of Wisconsin, Milwaukee, Wisconsin, United States of America.
authors: Avijit
authors: A
authors: Ray
authors: Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
authors: Cheng-Yin
authors: CY
authors: Yuan
authors: Blood Research Institute, BloodCenter of Wisconsin, Milwaukee, Wisconsin, United States of America.
authors: Nichole M
authors: NM
authors: Miller
authors: Blood Research Institute, BloodCenter of Wisconsin, Milwaukee, Wisconsin, United States of America.
authors: Hong
authors: H
authors: Mei
authors: Blood Research Institute, BloodCenter of Wisconsin, Milwaukee, Wisconsin, United States of America; Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
authors: Bonnie N
authors: BN
authors: Dittel
mesh_terms: D000818:Animals; D000917:Antibody Formation / Q000276:immunology*; D015703:Antigens, CD / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology*; D001853:Bone Marrow / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D007074:Immunoglobulin G / Q000276:immunology; D007075:Immunoglobulin M / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D010529:Peritoneal Cavity / Q000502:physiology*; D011971:Receptors, Immunologic / Q000276:immunology*; D000071176:Signaling Lymphocytic Activation Molecule Family
chemical_list: D015703:Antigens, CD; C490007:Cd244a protein, mouse; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D011971:Receptors, Immunologic; D000071176:Signaling Lymphocytic Activation Molecule Family