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Delineation of a defect in t-cell receptor beta-genes of nzw mice predisposed to autoimmunity

Academic Article
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Overview

authors

  • Noonan, D. J.
  • Kofler, R.
  • Singer, P. A.
  • Cardenas, G.
  • Dixon, F. J.
  • Theofilopoulos, Argyrios

publication date

  • March 1986

journal

  • Journal of Experimental Medicine  Journal

abstract

  • In an attempt to determine whether genes involved in T cell antigen recognition are structurally abnormal and thereby promote murine systemic lupus, we analyzed the structural integrity of the D, J, and C region elements of the T cell receptor alpha and beta chain genes in all major lupus strains and several normal strains. Within the limits of restriction fragment length polymorphism analysis, all strains had an identical genomic organization, except the NZW mice, in which a deletion of the C beta 1-D beta 2-J beta 2 elements was found. Sequence analysis of NZW genomic elements containing this deletion placed its probable origin within the first exon of C beta 1, and extending to a complementary region within the first exon of C beta 2. The significance of this abnormality in the pathogenesis of systemic autoimmune disease remains to be determined.

subject areas

  • Animals
  • Autoimmune Diseases
  • Base Sequence
  • Chromosome Deletion
  • Chromosome Mapping
  • DNA Restriction Enzymes
  • Genes
  • Genetic Linkage
  • Mice
  • Mice, Inbred Strains
  • Polymorphism, Genetic
  • Receptors, Antigen, T-Cell
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Identity

International Standard Serial Number (ISSN)

  • 0022-1007

Digital Object Identifier (DOI)

  • 10.1084/jem.163.3.644

PubMed ID

  • 3005467
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Additional Document Info

start page

  • 644

end page

  • 653

volume

  • 163

issue

  • 3

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