The Journal of Experimental Medicine
Rockland Immunochemicals for Research
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Published online April 9, 2007
doi:10.1084/jem.20062024
The Journal of Experimental Medicine, Vol. 204, No. 4, 747-758
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Waisman et al.
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ARTICLE

 IgG1 B cell receptor signaling is inhibited by CD22 and promotes the development of B cells whose survival is less dependent on Ig{alpha}/ß

Ari Waisman1, Manfred Kraus1,4,5, Jane Seagal4,5, Snigdha Ghosh6, Doron Melamed4,5,7, Jian Song1,2,3, Yoshiteru Sasaki4,5, Sabine Classen1, Claudia Lutz8, Frank Brombacher9, Lars Nitschke6, and Klaus Rajewsky1,4,5

1 Institute for Genetics and 2 Center for Molecular Medicine, University of Cologne, 50674 Cologne, Germany
3 I. Medical Department, Johannes Gutenberg-University Mainz, 55131 Mainz, Germany
4 CBR Institute for Biomedical Research and 5 Department of Pathology, Harvard Medical School, Boston, MA 02115
6 Department of Genetics, University of Erlangen, 91058 Erlangen, Germany
7 Department of Immunology, Ruth and Bruce Rappaport Faculty of Medicine and Rappaport Family Institute for Research in the Medical Sciences, Technion-Israel Institute of Technology, Haifa 31096, Israel
8 Max-Planck-Institute of Immunobiology, 79011 Freiburg, Germany
9 Department of Immunology, Groote Schuur Hospital, University of Cape Town, Cape Town 7925, South Africa

CORRESPONDENCE Klaus Rajewsky rajewsky{at}cbr.med.harvard.edu OR Ari Waisman: waisman{at}uni-mainz.de

We describe a mouse strain in which B cell development relies either on the expression of membrane-bound immunoglobulin (Ig) {gamma}1 or µ heavy chains. Progenitor cells expressing {gamma}1 chains from the beginning generate a peripheral B cell compartment of normal size with all subsets, but a partial block is seen at the pro– to pre–B cell transition. Accordingly, {gamma}1-driven B cell development is disfavored in competition with developing B cells expressing a wild-type (WT) IgH locus. However, the mutant B cells display a long half-life and accumulate in the mature B cell compartment, and even though partial truncation of the Ig{alpha} cytoplasmic tail compromises their development, it does not affect their maintenance, as it does in WT cells. IgG1-expressing B cells showed an enhanced Ca2+ response upon B cell receptor cross-linking, which was not due to a lack of inhibition by CD22. The enhanced Ca2+ response was also observed in mature B cells that had been switched from IgM to IgG1 expression in vivo. Collectively, these results suggest that the {gamma}1 chain can exert a unique signaling function that can partially replace that of the Ig{alpha}/ß heterodimer in B cell maintenance and may contribute to memory B cell physiology.

Abbreviations used: BAFF, B cell–activating factor; BCR, B cell receptor; C, constant region; CFSE, carboxyfluorescein succinimidyl ester; ERK, extracellular signal–related kinase; ES, embryonic stem; H, heavy; HRP, horseradish peroxidase; JNK, c-Jun N-terminal kinase; MZ, marginal zone; pBCR, pre-BCR; SHP-1, Src homology domain 2–containing protein tyrosine phosphatase; TLR, Toll-like receptor.

A. Waisman, M. Kraus, J. Seagal, L. Nitschke, and K. Rajewsky contributed equally to this work.

M. Kraus's present address is Merck Research Laboratories, Boston, MA 02115.


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