Dynamics and magnitude of virus-induced polyclonal B cell activation mediated by BCR-independent presentation of viral antigen
UMass Chan AffiliationsDepartment of Molecular Genetics and Microbiology
Program in Immunology and Virology
Department of Pathology
Graduate School of Biomedical Sciences
Document TypeJournal Article
KeywordsAmino Acid Sequence; Animals; Antibody-Producing Cells; *Antigen Presentation; Antigens, Viral; B-Lymphocyte Subsets; Cell Differentiation; Clone Cells; Histocompatibility Antigens Class II; Lymphocyte Activation; Lymphocytic Choriomeningitis; Lymphocytic choriomeningitis virus; Mice; Mice, Inbred C57BL; Mice, Knockout; Molecular Sequence Data; Receptors, Antigen, B-Cell
Medicine and Health Sciences
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AbstractHypergammaglobulinemia and production of autoantibodies occur during many viral infections, and studies have suggested that viral antigen-presenting B cells may become polyclonally activated by CD4 T cells in vivo in the absence of viral engagement of the BCR. However, we have reported that CD4 cells in lymphocytic choriomengitis virus (LCMV)-infected mice kill adoptively transferred B cells coated with LCMV class II peptides. We report here that most of the surviving naive B cells presenting class II MHC peptides undergo an extensive differentiation process involving both proliferation and secretion of antibodies. Both events require CD4 cells and CD40/CD40L interactions but not MyD88-dependent signaling within the B cells. B cells taken from immunologically tolerant donor LCMV-carrier mice with high LCMV antigen load became activated following adoptive transfer into LCMV-infected hosts, suggesting that B cells present sufficient antigen for this process during a viral infection. No division or activation of B cells was detected at all in virus-infected hosts in the absence of cognate CD4 T cells and class II antigen. This approach, therefore, formally demonstrates and quantifies a virus-induced polyclonal proliferation and differentiation of B cells, which, due to their high proportion, would mostly have BCR not specific for the virus.
SourceEur J Immunol. 2007 Jan;37(1):119-28. Link to article on publisher's site
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/33854
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