Abstract |
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.
|
Authors | Matthew J Colombo, David Abraham, Akira Shibuya, Kishore R Alugupalli |
Journal | Immunologic research
(Immunol Res)
Vol. 51
Issue 2-3
Pg. 249-56
(Dec 2011)
ISSN: 1559-0755 [Electronic] United States |
PMID | 22139824
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Review)
|
Chemical References |
- Antibodies, Bacterial
- Complement C3
- Immunoglobulin M
- Receptors, Fc
|
Topics |
- Adoptive Transfer
- Animals
- Antibodies, Bacterial
(immunology)
- Antibody-Dependent Cell Cytotoxicity
- B-Lymphocyte Subsets
(immunology)
- B-Lymphocytes
(immunology, transplantation)
- Borrelia
(immunology, pathogenicity)
- Borrelia Infections
(genetics, immunology)
- Cells, Cultured
- Complement C3
(genetics, immunology)
- Host-Pathogen Interactions
- Humans
- Immunoglobulin M
(immunology)
- Mice
- Phagocytosis
- Receptors, Fc
(immunology)
- Serum Bactericidal Antibody Assay
|