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Journal of Virology, June 2001, p. 5482-5490, Vol. 75, No. 12
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.12.5482-5490.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

B2 but Not B1 Cells Can Contribute to CD4+ T-Cell-Mediated Clearance of Rotavirus in SCID Mice

Natasha Kushnir,1 Nicolaas A. Bos,2 Adrian W. Zuercher,1 Susan E. Coffin,3 Charlotte A. Moser,3 Paul A. Offit,3 and John J. Cebra1,*

Department of Biology, University of Pennsylvania,1 and Division of Immunologic and Infectious Diseases, The Children's Hospital of Philadelphia,3 Philadelphia, Pennsylvania 19104, and Department of Histology and Cell Biology, University of Groningen, 9713 AV Groningen, The Netherlands2

Received 30 August 2000/Accepted 20 March 2001

Studies utilizing various immunodeficient mouse models of rotavirus (RV) infection demonstrated significant roles of RV-specific secretory immunoglobulin A (IgA), CD4+ T cells, and CD8+ T cells in the clearance of RV and protection from secondary infection. Secretion of small but detectable amounts of IgA in RV-infected alpha beta T-cell receptor knockout mice (11) and distinctive anatomical localization and physiology of B1 cells suggested that B1 cells might be capable of producing RV-specific intestinal IgA in a T-cell-independent fashion and, therefore, be responsible for ablation of RV shedding. We investigated the role of B1 cells in the resolution of primary RV infection using a SCID mouse model. We found that the adoptive transfer of unseparated peritoneal exudate cells ablates RV shedding and leads to the production of high levels of RV-specific intestinal IgA. In contrast, purified B1 cells do not ablate RV shedding and do not induce a T-cell-independent or T-cell-dependent, RV-specific IgA response but do secrete large amounts of polyclonal (total) intestinal IgA. Cotransfer of mixtures of purified B1 cells and B1-cell-depleted peritoneal exudate cells differing in IgA allotypic markers also demonstrated that B2 cells (B1-cell-depleted peritoneal exudate cells) and not B1 cells produced RV-specific IgA. To our knowledge, this is the first observation that B1 cells are unable to cooperate with CD4+ T cells and produce virus-specific intestinal IgA antibody. We also observed that transferred CD4+ T cells alone are capable of resolving RV shedding, although no IgA is secreted. These data suggest that RV-specific IgA may not be obligatory for RV clearance but may protect from reinfection and that effector CD4+ T cells alone can mediate the resolution of primary RV infection. Reconstitution of RV-infected SCID mice with B1 cells results in the outgrowth of contaminating, donor CD4+ T cells that are unable to clear RV, possibly because their oligoclonal specificities may be ineffective against RV antigens.

* Corresponding author. Mailing address: Department of Biology, University of Pennsylvania, Philadelphia, PA 19104-6018. Phone: (215) 898-5599. Fax: (215) 898-9786. E-mail: jcebra{at}sas.upenn.edu.

Journal of Virology, June 2001, p. 5482-5490, Vol. 75, No. 12
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.12.5482-5490.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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