The Journal of Experimental Medicine
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Published 6 May 2002. doi:10.1084/jem.20011550
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© Rockefeller University Press, 0022-1007/2002/5/1215/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 9, May 6, 2002 1215-1221

Brief Definitive Report

Very Low Affinity B Cells Form Germinal Centers, Become Memory B Cells, and Participate in Secondary Immune Responses When Higher Affinity Competition Is Reduced

Joseph M. Dal Porto1, Ann M. Haberman2, Garnett Kelsoe3 and Mark J. Shlomchik2

1 Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD 21201
2 Department of Laboratory Medicine and Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06510
3 Department of Immunology, Duke University Medical Center, Durham, NC 27710

Address correspondence to Mark J. Shlomchik, Department of Laboratory Medicine and Section of Immunobiology, Yale University School of Medicine, 330 Cedar St. Rm CB465, New Haven, CT 06510. Phone: 203-688-2089; Fax: 203-688-2748; E-mail: mark.shlomchik{at}yale.edu; or Garnett Kelsoe, Department of Immunology, Duke University Medical Center, 117 Jones Bldg., DUMC 3010, Research Dr., Durham, NC 27710. Phone: 919-613-7815; Fax: 919-613-7878; E-mail: ghkelsoe{at}duke.edu

To understand the relationship between the affinity of the B cell antigen receptor (BCR) and the immune response to antigen, two lines of immunoglobulin H chain transgenic (Tg) mice were created. H50Gµa and T1(V23)µa mice express µ H chain transgenes that associate with the {lambda}1 L chains to bind the (4-hydroxy-3-nitrophenyl)acetyl hapten with association constants (Kas) of only 1.2 x 105 M-1 and 3 x 104 M-1, respectively. Both lines mounted substantial antibody-forming cell (AFC) and germinal center (GC) responses. H50Gµa Tg mice also generated memory B cells. T1(V23)µa B cells formed AFC and GCs, but were largely replaced in late GCs by antigen-specific cells that express endogenous BCRs. Thus, B lymphocytes carrying BCRs with affinities previously thought to be irrelevant in specific immune responses are in fact capable of complete T cell–dependent immune responses when relieved of substantial competition from other B cells. The failure to observe such B cells normally in late primary responses and in memory B cell populations is the result of competition, rather than an intrinsic inability of low affinity B cells.

Key Words: mutation • antibody affinity • plasma cell • variable region gene • {lambda}1 immunoglobulin


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