Comparative contribution of CD1 on the development of CD4+ and CD8+ T cell compartments

Bin Wang, Taehoon Chun, Chyung Ru Wang

Research output: Contribution to journalArticle

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Abstract

CD1 molecules are MHC class I-like glycoproteins whose expression is essential for the development of a unique subset of T cells, the NK T cells. To evaluate to what extent CD1 contributes to the development of CD4+ and CD8+ T cells, we generated CD1°II°and CD1°TAP°mice and compared the generation of T cells in these double-mutant mice and II°or TAP°mice. FACS analysis showed that the number of CD4+ T cells in CD1°II°mice was reduced significantly compared with the corresponding population in II°mice. Both CD4+ NK1.1+ and the CD4+ NK1.1- population were reduced in CD1°II° mice, suggesting that CD1 can select not only CD4+ NK1.1+ T cells but also some NK1.1- CD4+ T cells. Functional analysis showed that the residual CD4+ cells in CD1°II°can secrete large amounts of IFN-γ and a significant amount of IL-4 during primary stimulation with anti-CD3, suggesting that this population may be enriched for NK T cells restricted by other class I molecules. In contrast to the CD4+ population, no significant differences in the CD8+ T cell compartment can be detected between TAP°and CD1°TAP° mice in all lymphoid tissues tested, including intestinal intraepithelial lymphocytes. Our data suggest that, unlike other MHC class I molecules, CD1 does not contribute in a major way to the development of CD8+ T cells.

Original languageEnglish
Pages (from-to)739-745
Number of pages7
JournalJournal of Immunology
Volume164
Issue number2
Publication statusPublished - 2000 Jan 15
Externally publishedYes

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T-Lymphocytes
Natural Killer Cells
Population
T-Lymphocyte Subsets
Lymphoid Tissue
Interleukin-4
Glycoproteins
Lymphocytes

ASJC Scopus subject areas

  • Immunology

Cite this

Comparative contribution of CD1 on the development of CD4+ and CD8+ T cell compartments. / Wang, Bin; Chun, Taehoon; Wang, Chyung Ru.

In: Journal of Immunology, Vol. 164, No. 2, 15.01.2000, p. 739-745.

Research output: Contribution to journalArticle

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