GSBS Student Publications

Title

Dynamics and magnitude of virus-induced polyclonal B cell activation mediated by BCR-independent presentation of viral antigen

GSBS Program

Biochemistry & Molecular Pharmacology

UMMS Affiliation

Graduate School of Biomedical Sciences; Department of Pathology; Program in Immunology and Virology; Department of Molecular Genetics and Microbiology

Date

12-14-2006

Document Type

Article

Medical Subject Headings

Amino 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

Disciplines

Life Sciences | Medicine and Health Sciences

Abstract

Hypergammaglobulinemia 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.

Rights and Permissions

Citation: Eur J Immunol. 2007 Jan;37(1):119-28. Link to article on publisher's site

Related Resources

Link to Article in PubMed

Journal Title

European journal of immunology

PubMed ID

17163452