The Journal of Experimental Medicine
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Published online 29 September 2003 doi:10.1084/jem.20021745
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© Rockefeller University Press, 0022-1007/2003/10/1011 $5.00
The Journal of Experimental Medicine, Volume 198, Number 7, 1011-1021

An Early CD4+ T Cell–dependent Immunoglobulin A Response to Influenza Infection in the Absence of Key Cognate T–B Interactions

Mark Y. Sangster1, Janice M. Riberdy2, Maricela Gonzalez1, David J. Topham3, Nicole Baumgarth4 and Peter C. Doherty1

1 Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105
2 Department of Hematology-Oncology, St. Jude Children's Research Hospital, Memphis, TN 38105
3 Center for Vaccine Biology and Immunology, University of Rochester Medical Center, Rochester, NY 14642
4 Center for Comparative Medicine, University of California, Davis, CA 95616

Address correspondence to Mark Y. Sangster, Department of Microbiology, M409 Walters Life Sciences Building, University of Tennessee, Knoxville, TN 37996. Phone: (865) 974-4028; Fax: (865) 974-4007; email: msangste{at}utk.edu

Contact-mediated interactions between CD4+ T cells and B cells are considered crucial for T cell–dependent B cell responses. To investigate the ability of activated CD4+ T cells to drive in vivo B cell responses in the absence of key cognate T–B interactions, we constructed radiation bone marrow chimeras in which CD4+ T cells would be activated by wild-type (WT) dendritic cells, but would interact with B cells that lacked expression of either major histocompatibility complex class II (MHC II) or CD40. B cell responses were assessed after influenza virus infection of the respiratory tract, which elicits a vigorous, CD4+ T cell–dependent antibody response in WT mice. The influenza-specific antibody response was strongly reduced in MHC II knockout and CD40 knockout mice. MHC II–deficient and CD40-deficient B cells in the chimera environment also produced little virus-specific immunoglobulin (Ig)M and IgG, but generated a strong virus-specific IgA response with virus-neutralizing activity. The IgA response was entirely influenza specific, in contrast to the IgG2a response, which had a substantial nonvirus-specific component. Our study demonstrates a CD4+ T cell–dependent, antiviral IgA response that is generated in the absence of B cell signaling via MHC II or CD40, and is restricted exclusively to virus-specific B cells.

Key Words: B lymphocytes • T lymphocytes • antibody formation • immunoglobulin A • mucosal immunity


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