Editing disease-associated autoantibodies

Ching Chen*, Eline Luning Prak, Martin Weigert

*Corresponding author for this work

Research output: Contribution to journalArticle

188 Scopus citations

Abstract

We have generated site-directed transgenic mice whose transgenes code for anti-DNA antibodies. These antibodies are representative of the lupus-associated anti-DNAs seen in mouse models of autoimmunity and human SLE, and have the usual characteristics of pathogenic autoantibodies. As conventional transgenics in nonautoimmune mice, anti-DNA B cells have been shown to be deleted or inactivated. Autoreactive B cells can also escape negative regulation by a process called receptor editing. Here we describe two combined immunoglobulin H and L chain site-directed transgenic mouse models and characterize their editing phenotypes. One model, 3H9R/Vκ4R, has a deletion-prone phenotype and undergoes editing, primarily by inactivation of the light chain by leap-frogging events. In the other model, 3H9R/Vκ8R, B cells are susceptible to anergy and maintain most of their HR and LR chains. These studies clarify the relationship between editing and other mechanisms of tolerance.

Original languageEnglish (US)
Pages (from-to)97-105
Number of pages9
JournalImmunity
Volume6
Issue number1
DOIs
StatePublished - Jan 1 1997

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

Fingerprint Dive into the research topics of 'Editing disease-associated autoantibodies'. Together they form a unique fingerprint.

  • Cite this