Title

Generation of protective T cell-independent antiviral antibody responses in SCID mice reconstituted with follicular or marginal zone B cells

PubMed ID

19542462

UMMS Affiliation

Department of Pathology; Department of Molecular Genetics and Microbiology

Date

6-23-2009

Document Type

Article

Subjects

Acute Disease; Adoptive Transfer; Animals; Antibodies, Viral; Antigens, T-Independent; B-Lymphocyte Subsets; Clone Cells; Immunoglobulin G; Immunoglobulin M; Immunophenotyping; Lymphoma, B-Cell, Marginal Zone; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, SCID; Polyomavirus Infections; Spleen; Survival Analysis; T-Lymphocyte Subsets

Disciplines

Life Sciences | Medicine and Health Sciences

Abstract

B cells generated in the bone marrow of adult mice enter the periphery as transitional B cells and subsequently differentiate into one of two phenotypically and functionally distinct subsets, marginal zone (MZ) or follicular (Fo) B cells. Recent reports indicate, however, that in response to environmental cues, such as lymphopenia, mature Fo B cells can change to display phenotypic markers characteristic of MZ B cells. Previously, we found that splenic B cells transferred to SCID mice responded to polyoma virus (PyV) infection with T cell-independent (TI) IgM and IgG secretion, reducing the viral load and protecting mice from the lethal effect of the infection. The contribution of MZ and Fo B cell subsets to this antiviral TI-2 response, however, has not been addressed. In this study, we show that both sort-purified MZ and Fo B cells generate protective TI Ab responses to PyV infection when transferred into SCID mice. Moreover, the transferred Fo B cells in the spleens of the PyV-infected SCID mice change phenotype, with many of them displaying MZ B cell characteristics. These findings demonstrate the plasticity of the B cell subsets in virus-infected hosts and show for the first time that B cells derived exclusively from Fo B cells can effectively function in antiviral TI-2 responses.

Rights and Permissions

Citation: J Immunol. 2009 Jul 1;183(1):518-23. Link to article on publisher's site

Related Resources

Link to Article in PubMed