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Thymocyte resistance to glucocorticoids leads to antigen-specific unresponsiveness due to "holes" in the t cell repertoire

Academic Article
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Overview

authors

  • Lu, F. W. M.
  • Yasutomo, K.
  • Goodman, G. B.
  • McHeyzer-Williams, L. J.
  • McHeyzer-Williams, Michael G.
  • Germain, R. N.
  • Ashwell, J. D.

publication date

  • February 2000

journal

  • Immunity  Journal

abstract

  • We have proposed that glucocorticoids antagonize TCR-mediated activation and influence which TCR avidities result in positive or negative selection. We now analyze the immune response of mice whose thymocytes express antisense transcripts to the glucocorticoid receptor (TKO mice). TKO mice responded normally to the complex antigen PPD but were proliferative nonresponders to pigeon cytochrome c 81-104 (PCC), having a large decrease in the frequency of PCC-responsive CD4+ T cells. Unlike wild-type T cells, few TKO T cells in PCC-specific cell lines expressed V alpha11+Vbeta3+. Furthermore, for naive CD4+ T cells from unimmunized TKO mice, the frequencies of many of the molecular features common to the CDR3 regions of PCC-responsive V alpha11+Vbeta3+ cells were substantially decreased. Thus, thymocyte glucocorticoid hyporesponsiveness resulted in loss of cells capable of responding to PCC, corresponding to an antigen-specific "hole" in the T cell repertoire.

subject areas

  • Animals
  • Cell Line
  • Cytochrome c Group
  • Female
  • Glucocorticoids
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Receptors, Antigen, T-Cell, alpha-beta
  • Receptors, Glucocorticoid
  • T-Lymphocytes
  • Thymus Gland
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Identity

International Standard Serial Number (ISSN)

  • 1074-7613

Digital Object Identifier (DOI)

  • 10.1016/s1074-7613(00)80171-5

PubMed ID

  • 10714684
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Additional Document Info

start page

  • 183

end page

  • 192

volume

  • 12

issue

  • 2

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