title: Ligation of CD27 on murine B cells responding to T-dependent and T-independent stimuli inhibits the generation of plasma cells.
abstract: B cells can be stimulated either allogenically with the Th cell clone D10G4.1 and bone marrow-derived dendritic cells or polyclonally with LPS to proliferate and undergo terminal differentiation to Ig-secreting plasma cells in vitro. The addition of anti-CD27 to such cultures inhibits Ig secretion, and inhibition is more marked in T-dependent cultures than in T-independent cultures. Both IgM and secondary isotypes are affected, and addition of anti-CD27 even 4 days after culture initiation inhibits Ig secretion. Anti-CD27 does not affect B cell proliferation or the acquisition of activation markers by B cells, and no marked loss of B cell viability is detected in cells cultured in the presence of anti-CD27, suggesting that the inhibition of Ig secretion is not due to inhibition of early activation events or to death of activated cells in vitro. However, the presence of anti-CD27 significantly inhibits the induction of Blimp-1 and J chain transcripts, which are turned on in cells committed to plasma cell differentiation. Furthermore, mice immunized under cover of anti-CD27 make less Ag-specific IgM and IgG, but have equivalent T cell responses when compared with control mice. These data suggest that ligation of CD27, a member of the TNFR family, on the B cell surface may prevent terminal differentiation of activated B cells into Ig-secreting plasma cells.
authors: National Institute of Immunology, New Delhi, India.
authors: V S
authors: VS
authors: Raman
authors: V
authors: V
authors: Bal
authors: S
authors: S
authors: Rath
authors: A
authors: A
authors: George
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000494:pharmacology; D015703:Antigens, CD / Q000096:biosynthesis; D000955:Antigens, T-Independent / Q000502:physiology*; D001402:B-Lymphocytes / Q000166:cytology / Q000276:immunology* / Q000378:metabolism*; D015415:Biomarkers; D051927:CD24 Antigen; D002454:Cell Differentiation / Q000276:immunology; D002470:Cell Survival / Q000276:immunology; D002478:Cells, Cultured; D006131:Growth Inhibitors / Q000502:physiology; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis; D018960:Hyaluronan Receptors / Q000096:biosynthesis; D007136:Immunoglobulins / Q000096:biosynthesis; D007166:Immunosuppressive Agents / Q000494:pharmacology; D007279:Injections, Subcutaneous; D008024:Ligands; D008070:Lipopolysaccharides / Q000494:pharmacology; D008213:Lymphocyte Activation; D008562:Membrane Glycoproteins; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D010950:Plasma Cells / Q000166:cytology* / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7 / Q000276:immunology* / Q000378:metabolism*
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D000955:Antigens, T-Independent; D015415:Biomarkers; D051927:CD24 Antigen; C497890:Cd24a protein, mouse; D006131:Growth Inhibitors; D000949:Histocompatibility Antigens Class II; D018960:Hyaluronan Receptors; D007136:Immunoglobulins; D007166:Immunosuppressive Agents; D008024:Ligands; D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7