B cell development is often portrayed as a series of decision points that expand an antigen-reactive cell to a clone producing a single antibody. This is hardly the case: B cell development is dependent on a series of error-prone, random rearrangement events that through ongoing diversification reach a compromise in which most cells are not autoreactive (except in disease) and the majority of clone members remain specific for the initial antigen. One familiar example of ongoing diversification is somatic mutation during clonal expansion 1. Another example, receptor editing, is the means by which immature bone marrow B cells become self-tolerant 2,3,4. Here rearrangements are induced by encounter with autoantigens to change specificity from self to non-self. Now, a third level of diversification, termed “receptor revision,” has been suggested to occur in mature B...
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Commentary|
May 30 2000
Revising B Cell Receptors
David Nemazee,
David Nemazee
aThe Scripps Research Institute, La Jolla, California 92037
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Martin Weigert
Martin Weigert
bDepartment of Molecular Biology, Princeton University, Princeton, New Jersey 08544
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David Nemazee
aThe Scripps Research Institute, La Jolla, California 92037
Martin Weigert
bDepartment of Molecular Biology, Princeton University, Princeton, New Jersey 08544
Received:
April 10 2000
Accepted:
April 21 2000
Online ISSN: 1540-9538
Print ISSN: 0022-1007
© 2000 The Rockefeller University Press
2000
The Rockefeller University Press
J Exp Med (2000) 191 (11): 1813–1818.
Article history
Received:
April 10 2000
Accepted:
April 21 2000
Citation
David Nemazee, Martin Weigert; Revising B Cell Receptors. J Exp Med 5 June 2000; 191 (11): 1813–1818. doi: https://doi.org/10.1084/jem.191.11.1813
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