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

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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.

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Acknowledgments

We thank Jessica Hess and Sandra Bonne-Année for assistance with diffusion chamber experiments, Dr. Robert Eisenberg for providing C3−/− mice and Dr. Utpal Pal for reviewing the manuscript. This work was supported by NIH grant R01 AI065750 to KRA and 1R56AI076345 to DA.

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Correspondence to Kishore R. Alugupalli.

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Colombo, M.J., Abraham, D., Shibuya, A. et al. B1b lymphocyte-derived antibodies control Borrelia hermsii independent of Fcα/μ receptor and in the absence of host cell contact. Immunol Res 51, 249–256 (2011). https://doi.org/10.1007/s12026-011-8260-8

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  • DOI: https://doi.org/10.1007/s12026-011-8260-8

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