IgD can largely substitute for loss of IgM function in B cells

Claudia Lutz, Birgit Ledermann, Marie H. Kosco-Vilbois, Adrian F. Ochsenbein, Rolf M. Zinkernagel, Georges Köhler and Frank Brombacher ()
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Claudia Lutz: Max-Planck-Institute for Immunobiology
Birgit Ledermann: Novartis Pharma Inc., Research
Marie H. Kosco-Vilbois: Geneva Biomedical Research Institute, Glaxo Welcome Research and Development
Adrian F. Ochsenbein: Institute for Experimental Immunology
Rolf M. Zinkernagel: Institute for Experimental Immunology
Georges Köhler: Max-Planck-Institute for Immunobiology
Frank Brombacher: Max-Planck-Institute for Immunobiology

Nature, 1998, vol. 393, issue 6687, 797-801

Abstract: Abstract The μ and δ heavy chains of IgM and IgD, the first antibody isotypes expressed during bone-marrow B-cell development, are encoded by a common transcription unit. Expression of the μ chain on the surface of late pre-B cells allows their further development to immature B cells. Coexpression of the δ chain and emigration of the immature B cells to the periphery eventually leads to the development of naive mature IgM/IgD double-positive cells. Although IgM is important in driving B-cell development1, the contribution of IgD is not clear. Here we investigate the function of IgD. We generated mice deficient in IgM (IgM−/− mice) by deleting the μ region in embryonic stem cells. IgM−/− mice showed normal B-cell development and maturation, with IgD replacing membrane-bound and secretory IgM. Moreover, specific B-cell responses and isotype class switches occurred during immunization or infection. In contrast to mice deficient in B cells, IgM−/− mice survived infection with vesicular stomatitis virus by developing neutralizing immunoglobulins, but they were more susceptible than wild-type controls with delayed specific immunoglobulin responses. These data lead us to conclude that IgD is largely able to substitute for IgM functions.

Date: 1998
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DOI: 10.1038/31716

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