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Self-antigen does not accelerate immature b cell apoptosis, but stimulates receptor editing as a consequence of developmental arrest

Academic Article
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Overview

authors

  • Melamed, D.
  • Nemazee, David

publication date

  • August 1997

journal

  • Proceedings of the National Academy of Sciences of the United States of America  Journal

abstract

  • In pre-B lymphocytes, productive rearrangement of Ig light chain genes allows assembly of the B cell receptor (BCR), which selectively promotes further developmental maturation through poorly defined transmembrane signaling events. Using a novel in vitro system to study immune tolerance during development, we find that BCR reactivity to auto-antigen blocks this positive selection, preventing down-regulation of light chain gene recombination and promoting secondary light chain gene rearrangements that often alter BCR specificity, a process called receptor editing. Under these experimental conditions, self-antigen induces secondary light chain gene rearrangements in at least two-thirds of autoreactive immature B cells, but fails to accelerate cell death at this stage. These data suggest that in these cells the mechanism of immune tolerance is receptor selection rather than clonal selection.

subject areas

  • Animals
  • Apoptosis
  • Autoantigens
  • B-Lymphocytes
  • Cell Differentiation
  • Immune Tolerance
  • Mice
  • Receptors, Antigen, B-Cell
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Identity

International Standard Serial Number (ISSN)

  • 0027-8424

Digital Object Identifier (DOI)

  • 10.1073/pnas.94.17.9267

PubMed ID

  • 9256471
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Additional Document Info

start page

  • 9267

end page

  • 9272

volume

  • 94

issue

  • 17

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