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Tolerance-related v-beta clonal deletions in normal cd4-8-, tcr-alpha/beta+ and abnormal lpr and gld cell-populations

Academic Article
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Overview

authors

  • Singer, P. A.
  • Balderas, R. S.
  • McEvilly, R. J.
  • Bobardt, M.
  • Theofilopoulos, Argyrios

publication date

  • 1989

journal

  • Journal of Experimental Medicine  Journal

abstract

  • We have analyzed tolerance-related clonal deletion of Mls-and I-E-reactive thymocytes at the RNA level using a multi-V beta probe RNAse protection assay, and used this phenomenon to identify the maturation stage of the abnormally expanded CD4-8-, TCR-alpha/beta + subset in lpr and gld homozygous mice, and of the phenotypically similar minor thymocyte subset found in normal mice. Essentially complete V beta clonal deletions were detected in lpr and gld cells of all appropriate background strains. Substantial, but not complete, V beta clonal deletions were also detected in the CD4-8- TCR-alpha/beta + subset of normal mice. Since expression of CD4/CD8 is required for V beta clonal deletions to occur, we conclude that lpr and gld cells, and at least a portion of CD4-8- TCR-alpha/beta + thymocytes in normal mice, are derived by secondary loss of CD4/CD8 accessory molecules from more mature CD4+8+ precursors. One possible interpretation of these findings is that such CD4/CD8 loss may affect a class of self-reactive thymocytes that have escaped direct clonal deletion. Exportation and expansion of such cells in the periphery may be an important contributory factor in the induction of systemic autoimmunity.

subject areas

  • Animals
  • Antigens, CD4
  • Antigens, CD8
  • Antigens, Differentiation, T-Lymphocyte
  • Autoimmune Diseases
  • Chromosome Deletion
  • Immune Tolerance
  • Lymphoproliferative Disorders
  • Mice
  • Mice, Inbred C3H
  • RNA, Messenger
  • Receptors, Antigen, T-Cell
  • T-Lymphocytes
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Identity

International Standard Serial Number (ISSN)

  • 0022-1007

Digital Object Identifier (DOI)

  • 10.1084/jem.170.6.1869

PubMed ID

  • 2511266
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Additional Document Info

start page

  • 1869

end page

  • 1877

volume

  • 170

issue

  • 6

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