Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form
As of April 1st VIVO Scientific Profiles will no longer updated for faculty, and the link to VIVO will be removed from the library website. Faculty profile pages will continue to be updated via Interfolio. VIVO will continue being used behind the scenes to update graduate student profiles. Please contact helplib@scripps.edu if you have questions.
How to download citations from VIVO | Alternative profile options

Enforced bcl-2 expression inhibits antigen-mediated clonal elimination of peripheral b cells in an antigen dose-dependent manner and promotes receptor editing in autoreactive, immature b cells

Academic Article
uri icon
  • Overview
  • Identity
  • Additional Document Info
  • View All
scroll to property group menus

Overview

authors

  • Lang, J.
  • Arnold, B.
  • Hammerling, G.
  • Harris, A. W.
  • Korsmeyer, S.
  • Russell, D.
  • Strasser, A.
  • Nemazee, David

publication date

  • November 1997

journal

  • Journal of Experimental Medicine  Journal

abstract

  • The mechanisms that establish immune tolerance in immature and mature B cells appear to be distinct. Membrane-bound autoantigen is thought to induce developmental arrest and receptor editing in immature B cells, whereas mature B cells have shortened lifespans when exposed to the same stimulus. In this study, we used Emu-bcl-2-22 transgenic (Tg) mice to test the prediction that enforced expression of the Bcl-2 apoptotic inhibitor in B cells would rescue mature, but not immature, B cells from tolerance induction. To monitor tolerance to the natural membrane autoantigen H-2Kb, we bred 3-83mudelta (anti-Kk,b) Ig Tg mice to H-2(b) mice or to mice expressing transgene-driven Kb in the periphery. In 3-83mudelta/bcl-2 Tg mice, deletion of autoreactive B cells induced by peripheral Kb antigen expression in the liver (MT-Kb Tg) or epithelia (KerIV-Kb Tg), was partly or completely inhibited, respectively. Furthermore, Bcl-2 protected peritoneal B-2 B cells from deletion mediated by acute antigen exposure, but this protection could be overcome by higher antigen dose. In contrast to its ability to block peripheral self-tolerance, Bcl-2 overexpression failed to inhibit central tolerance induced by bone marrow antigen expression, but instead, enhanced the receptor editing process. These studies indicate that apoptosis plays distinct roles in central and peripheral B cell tolerance.

subject areas

  • Animals
  • Antibodies, Anti-Idiotypic
  • Antigens, CD45
  • B-Lymphocyte Subsets
  • Cell Differentiation
  • Cell Survival
  • Clonal Deletion
  • Dose-Response Relationship, Immunologic
  • Epithelial Cells
  • Gene Rearrangement, B-Lymphocyte, Light Chain
  • H-2 Antigens
  • Hybridomas
  • Immunoglobulin M
  • Immunoglobulin kappa-Chains
  • Immunoglobulin lambda-Chains
  • Injections, Intraperitoneal
  • Liver
  • Lymphocyte Count
  • Lymphoid Tissue
  • Mice
  • Mice, Inbred A
  • Mice, Inbred C3H
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Transgenic
  • Proto-Oncogene Proteins c-bcl-2
scroll to property group menus

Identity

International Standard Serial Number (ISSN)

  • 0022-1007

Digital Object Identifier (DOI)

  • 10.1084/jem.186.9.1513

PubMed ID

  • 9348309
scroll to property group menus

Additional Document Info

start page

  • 1513

end page

  • 1522

volume

  • 186

issue

  • 9

©2022 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support