CD8 lineage commitment in the absence of CD8

Immunity. 1997 May;6(5):633-42. doi: 10.1016/s1074-7613(00)80351-9.

Abstract

The absence of cytotoxic T lymphocyte activity and the failure of MHC class I-restricted T cell receptor (TCR) transgenic thymocytes to mature in CD8alpha-deficient mice suggest that CD8 may be essential for CD8 lineage commitment. We report that variants of the antigenic peptide that delete TCR transgenic thymocytes from CD8 wild-type but not CD8alpha-deficient mice can restore positive selection of CD8 lineage cells in the absence of CD8. The positively selected cells down-regulate CD4, up-regulate TCR, respond to the antigenic peptide, and express CD8beta mRNA. Interestingly, there was no enhanced selection of CD4+ T cells, implying that the TCR-MHC interaction, even in the absence of CD8, provided instructive signaling for commitment to the CD8 lineage. Our results are discussed in terms of recent models of T cell lineage commitment.

Publication types

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

MeSH terms

  • Animals
  • CD8 Antigens / genetics*
  • CD8-Positive T-Lymphocytes / cytology
  • CD8-Positive T-Lymphocytes / immunology*
  • CD8-Positive T-Lymphocytes / metabolism*
  • Cell Differentiation / genetics
  • Cell Differentiation / immunology
  • Clonal Deletion
  • Fetus
  • Genetic Variation
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Organ Culture Techniques
  • Ovalbumin / genetics
  • Ovalbumin / immunology
  • Peptides / genetics
  • Peptides / immunology
  • RNA, Messenger / biosynthesis
  • Receptors, Antigen, T-Cell / genetics
  • Thymus Gland / cytology

Substances

  • CD8 Antigens
  • Peptides
  • RNA, Messenger
  • Receptors, Antigen, T-Cell
  • Ovalbumin