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B7 expression on thymic medullary epithelium correlates with epithelium-mediated deletion of v-beta-5(+) thymocytes

Academic Article
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Overview

authors

  • Degermann, S.
  • Surh, Charles
  • Glimcher, L. H.
  • Sprent, Jonathan
  • Lo, D.

publication date

  • April 1994

journal

  • Journal of Immunology  Journal

abstract

  • Recent evidence suggests that I-E+ thymic epithelium, especially medullary epithelium, can induce partial deletion of superantigen-reactive T cells expressing TcR V beta 5, V beta 11, and V beta 17. To seek further information on this issue, we constructed bone marrow chimeras in which MHC class II I-E is expressed on thymic epithelial cells at various levels and locations; the chimeras were reconstituted with stem cells from TcR V beta 5 transgenic mice. Intrathymic deletion of V beta 5 T cells was restricted to relatively mature T cells (expressing high TcR levels), and the degree of deletion correlated with the density of I-E expression in the thymic medulla rather than in the thymic cortex; selective I-E expression in medullary epithelium caused prominent deletion. Interestingly, immunostaining of normal and chimeric mice revealed that expression of B7 (the ligand for CD28) is largely restricted to a subset of medullary epithelial cells; these cells are I-E+ and co-express a specific carbohydrate bound by the lectin UEA-1. B7 expression was lower in thymuses of class II-deficient mice (A beta b-/-) and T-cell-deficient mice (SCID), suggesting that B7 expression is up-regulated during CD4+ thymocyte selection. In support of this idea, B7 expression in the thymus was restored to a normal level in bone marrow reconstituted SCID mice. Because B7 expression correlates with a costimulatory signal for T cells, selective expression of B7 and related antigens on I-E+ medullary epithelium may explain why these cells play a more prominent role in V beta deletion than cortical epithelium.

subject areas

  • Animals
  • Antigens, CD80
  • CD4-Positive T-Lymphocytes
  • Histocompatibility Antigens Class II
  • Lectins
  • Lymphocyte Depletion
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, SCID
  • Plant Lectins
  • Receptors, Antigen, T-Cell, alpha-beta
  • T-Lymphocyte Subsets
  • Thymus Gland
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Identity

International Standard Serial Number (ISSN)

  • 0022-1767

PubMed ID

  • 7511640
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Additional Document Info

start page

  • 3254

end page

  • 3263

volume

  • 152

issue

  • 7

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