Why is clonal deletion of neonatal thymocytes defective?

Eur J Immunol. 1992 Oct;22(10):2487-93. doi: 10.1002/eji.1830221004.

Abstract

A major mechanism for establishing tolerance to some murine self antigens is clonal deletion of self reactive T cells in the thymus. This mechanism is responsible for the near absence of T cells displaying particular T cell receptor (TcR) V beta in strains of mice that express the major histocompatibility complex class II E molecule and a protein encoded within the 3' open reading frame (ORF) of certain endogenous mammary tumor viruses (Mtv). However, clonal deletion does not operate in these same strains during the first few days after birth. This defect could be explained by a difference in any (or any combination of) the three elements involved: the T cell, the thymic stromal cell(s) or the antigen. We have explored these different possibilities and have come to the conclusion that a lack of antigen is the most likely explanation. Yet, neonatal and adult thymi have quite similar levels of messenger ribonucleic acid corresponding to Mtv 3' ORF.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Animals, Newborn / immunology*
  • Base Sequence
  • CD4 Antigens / analysis
  • CD8 Antigens / analysis
  • Enterotoxins / pharmacology
  • Immune Tolerance*
  • Mammary Tumor Virus, Mouse / genetics
  • Mice
  • Mice, Transgenic
  • Molecular Sequence Data
  • Open Reading Frames
  • Receptors, Antigen, T-Cell, alpha-beta / analysis
  • Receptors, Antigen, T-Cell, alpha-beta / genetics
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology*

Substances

  • CD4 Antigens
  • CD8 Antigens
  • Enterotoxins
  • Receptors, Antigen, T-Cell, alpha-beta
  • enterotoxin B, staphylococcal