Receptor editing : an approach by autoreactive B cells to escape tolerance
To determine the fate of anti-DNA antibody-bearing B cells in normal mice, we generated transgenic mice bearing the heavy (H) and light (L) chain genes of a well-characterized anti-double-stranded DNA antibody. This antibody was originally isolated from a diseased MRL/lpr mouse and has characteristi...
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Published in | The Journal of experimental medicine Vol. 177; no. 4; pp. 999 - 1008 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
New York, NY
Rockefeller University Press
01.04.1993
The Rockefeller University Press |
Subjects | |
Online Access | Get full text |
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Abstract | To determine the fate of anti-DNA antibody-bearing B cells in normal mice, we generated transgenic mice bearing the heavy (H) and light (L) chain genes of a well-characterized anti-double-stranded DNA antibody. This antibody was originally isolated from a diseased MRL/lpr mouse and has characteristics common to spontaneously arising anti-DNA antibodies. Results show that the H/L transgene (tg) immunoglobulin receptor is not expressed by animals bearing both tgs, although single tg animals (H or L) express their transgenes. Young H/L tg animals express few B cells, whereas adult H/L tg animals maintain almost normal B cell numbers. Analysis of the immunoglobulin receptors used by adult B cells shows that all contain the tg H chain in association with endogenous L chains. These B cells transcribe the L tg as well as the rearranged endogenous L chain gene, and loss of endogenous L chain gene transcription results in resurrection of the 3H9 H/L tg product. Examination of the endogenous L chains used by these cells shows that they represent a highly restricted subset of V genes. Taken together, these data suggest that autoreactive transgenic B cells can rearrange endogenous L chain genes to alter surface receptors. Those L chains that compete successfully with the L tg for H chain binding, and that create a nonautoreactive receptor, allow the B cell to escape deletion. We suggest that this receptor editing is a mechanism used by immature autoreactive B cells to escape tolerance. |
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AbstractList | To determine the fate of anti-DNA antibody-bearing B cells in normal mice, we generated transgenic mice bearing the heavy (H) and light (L) chain genes of a well-characterized anti-double-stranded DNA antibody. This antibody was originally isolated from a diseased MRL/lpr mouse and has characteristics common to spontaneously arising anti-DNA antibodies. Results show that the H/L transgene (tg) immunoglobulin receptor is not expressed by animals bearing both tgs, although single tg animals (H or L) express their transgenes. The data suggest that autoreactive transgenic B cells can rearrange endogenous L chain genes to alter surface receptors. Those L chains that compete successfully with the L tg for H chain binding, and that create a nonautoreactive receptor, allow the B cell to escape deletion. We suggest that this receptor editing is a mechanism used by immature autoreactive B cells to escape tolerance. To determine the fate of anti-DNA antibody-bearing B cells in normal mice, we generated transgenic mice bearing the heavy (H) and light (L) chain genes of a well-characterized anti-double-stranded DNA antibody. This antibody was originally isolated from a diseased MRL/lpr mouse and has characteristics common to spontaneously arising anti-DNA antibodies. Results show that the H/L transgene (tg) immunoglobulin receptor is not expressed by animals bearing both tgs, although single tg animals (H or L) express their transgenes. Young H/L tg animals express few B cells, whereas adult H/L tg animals maintain almost normal B cell numbers. Analysis of the immunoglobulin receptors used by adult B cells shows that all contain the tg H chain in association with endogenous L chains. These B cells transcribe the L tg as well as the rearranged endogenous L chain gene, and loss of endogenous L chain gene transcription results in resurrection of the 3H9 H/L tg product. Examination of the endogenous L chains used by these cells shows that they represent a highly restricted subset of V genes. Taken together, these data suggest that autoreactive transgenic B cells can rearrange endogenous L chain genes to alter surface receptors. Those L chains that compete successfully with the L tg for H chain binding, and that create a nonautoreactive receptor, allow the B cell to escape deletion. We suggest that this receptor editing is a mechanism used by immature autoreactive B cells to escape tolerance. |
Author | CAMPER, S GAY, D WEIGERT, M SAUNDERS, T |
Author_xml | – sequence: 1 givenname: D surname: GAY fullname: GAY, D organization: Fox Chase cancer cent., inst. cancer res., Philadelphia PA 19111, United States – sequence: 2 givenname: T surname: SAUNDERS fullname: SAUNDERS, T organization: Fox Chase cancer cent., inst. cancer res., Philadelphia PA 19111, United States – sequence: 3 givenname: S surname: CAMPER fullname: CAMPER, S organization: Fox Chase cancer cent., inst. cancer res., Philadelphia PA 19111, United States – sequence: 4 givenname: M surname: WEIGERT fullname: WEIGERT, M organization: Fox Chase cancer cent., inst. cancer res., Philadelphia PA 19111, United States |
BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4717946$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/8459227$$D View this record in MEDLINE/PubMed |
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Keywords | Autoimmunity Immunoglobulins heavy-Peptide chain Rodentia Transgenic animal Autoantibody light-Peptide chain B-Lymphocyte Vertebrata Double stranded DNA Specificity Mammalia Gene Mouse Immune tolerance Biological receptor |
Language | English |
License | CC BY 4.0 This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
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Snippet | To determine the fate of anti-DNA antibody-bearing B cells in normal mice, we generated transgenic mice bearing the heavy (H) and light (L) chain genes of a... |
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SubjectTerms | Animals Autoantibodies - genetics Autoantibodies - immunology Autoimmunity (experimental aspects and models) B-Lymphocytes - immunology Base Sequence Biological and medical sciences Blotting, Southern Cell Line DNA - immunology Flow Cytometry Fundamental and applied biological sciences. Psychology Fundamental immunology Hybridomas Immune Tolerance Immunoglobulin Heavy Chains - genetics Immunoglobulin Heavy Chains - immunology Immunoglobulin Heavy Chains - metabolism Immunoglobulin Light Chains - genetics Immunoglobulin Light Chains - immunology Immunoglobulin Light Chains - metabolism Mice Mice, Inbred BALB C Mice, Transgenic Molecular Sequence Data Receptors, Antigen, B-Cell - immunology Receptors, Antigen, B-Cell - metabolism Restriction Mapping |
Title | Receptor editing : an approach by autoreactive B cells to escape tolerance |
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