B1b lymphocyte-derived antibodies control Borrelia hermsii independent of Fcα/μ receptor and in the absence of host cell contact

• Published in: Immunologic research 2011-12, Vol.51 (2-3), p.249-256
• Main Authors: Colombo, Matthew J., Abraham, David, Shibuya, Akira, Alugupalli, Kishore R.
• Format: Article
• Language: English
• Subjects: Adoptive Transfer; Allergology; Animal models; Animals; Antibodies, Bacterial - immunology; Antibody-Dependent Cell Cytotoxicity; B-Lymphocyte Subsets - immunology; B-Lymphocytes - immunology; B-Lymphocytes - transplantation; Bacteremia; Biomedical and Life Sciences; Biomedicine; Borrelia - immunology; Borrelia - pathogenicity; Borrelia hermsii; Borrelia Infections - genetics; Borrelia Infections - immunology; Cells, Cultured; Complement activation; Complement C3 - genetics; Complement C3 - immunology; Current Immunology Research at Jefferson; Diffusion chambers; Host-Pathogen Interactions; Humans; Immunoglobulin M; Immunoglobulin M - immunology; Immunology; Infection; Internal Medicine; Medicine/Public Health; Mice; opsonophagocytosis; Pathogens; Phagocytosis; Pores; Receptors, Fc - immunology; Serum Bactericidal Antibody Assay
• ISSN: 0257-277X; 1559-0755
• DOI: 10.1007/s12026-011-8260-8

The critical role of IgM in controlling pathogen burden has been demonstrated in a variety of infection models. In the murine model of Borrelia hermsii infection, IgM is necessary and sufficient for the rapid clearance of bacteremia. Convalescent, but not naïve, B1b cells generate a specific IgM response against B. hermsii , but the mechanism of IgM-mediated protection is unknown. Here, we show that neither Fcα/μR, a high-affinity receptor for IgM, nor IgM-dependent complement activation is required for controlling B. hermsii . Bacteria in diffusion chambers with a pore size impermeable to cells were killed when diffusion chambers were implanted into either convalescent or passively immunized mice. Furthermore, adoptively transferred convalescent B1b cells in Rag1 −/− mice produced specific IgM that also cleared B. hermsii in diffusion chambers independent of complement. These results demonstrate that IgM-mediated clearance of B. hermsii does not require opsonophagocytosis and indicate that a mechanism for in vivo B1b cell-mediated protection is through the generation of bactericidal IgM.