CD3+ WT31- peripheral T lymphocytes lack T44 (CD28), a surface molecule involved in activation of T cells bearing the α/β heterodimer

A. Poggi, C. Bottino, M. R. Zocchi, G. Pantaleo, E. Ciccone, C. Mingari, L. Moretta, A. Moretta

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Abstract

We have applied two-color fluorescence cytofluorometric techniques to the analysis of the distribution of T44 and CD3 antigens in peripheral blood human lymphocytes. While most CD3+ cells co-expressed T44 antigen, a small distinct subset was CD3+ T44- (2-10% of CD3+ cells). This cell subset also did not react with the WT31 monoclonal antibody (mAb), specific for an α/β framework determinant of the T cell receptor (TCR). Lack of T44 antigen expression was also observed in purified CD3+ WT31- polyclonal populations that had been cultured in medium containing interleukin 2 (IL 2) and as well as >30 clones expressing the CD3+4-8-WT31- surface phenotype. Immunoprecipitation experiments confirmed that expression of T44 molecules was confined to CD3+ WT31+ peripheral blood T cells. While conventional CD3+ WT31+ cells produced IL 2 in response to mAb directed to CD2, CD3 or T44 surface molecules, CD3+ WT31- cells did not respond to anti-T44 mAb but released IL 2 following stimulation with anti-CD2 or anti-CD3 mAb. Therefore, assuming that anti-T44 mimicks the effect of a still undefined natural ligand our data suggest that T cells expressing the γ-gene surface product may be signalled by stimuli which differ, at least in part, from those acting on CD3+ WT31+ T lymphocytes.

Original languageEnglish
Pages (from-to)1065-1068
Number of pages4
JournalEuropean Journal of Immunology
Volume17
Issue number7
DOIs
Publication statusPublished - 1987

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T-Lymphocytes
Monoclonal Antibodies
Interleukin-2
CD3 Antigens
Antigens
T-Cell Antigen Receptor
Immunoprecipitation
Blood Cells
Clone Cells
Color
Fluorescence
Lymphocytes
Ligands
Phenotype
Population
Genes

ASJC Scopus subject areas

  • Immunology

Cite this

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title = "CD3+ WT31- peripheral T lymphocytes lack T44 (CD28), a surface molecule involved in activation of T cells bearing the α/β heterodimer",
abstract = "We have applied two-color fluorescence cytofluorometric techniques to the analysis of the distribution of T44 and CD3 antigens in peripheral blood human lymphocytes. While most CD3+ cells co-expressed T44 antigen, a small distinct subset was CD3+ T44- (2-10{\%} of CD3+ cells). This cell subset also did not react with the WT31 monoclonal antibody (mAb), specific for an α/β framework determinant of the T cell receptor (TCR). Lack of T44 antigen expression was also observed in purified CD3+ WT31- polyclonal populations that had been cultured in medium containing interleukin 2 (IL 2) and as well as >30 clones expressing the CD3+4-8-WT31- surface phenotype. Immunoprecipitation experiments confirmed that expression of T44 molecules was confined to CD3+ WT31+ peripheral blood T cells. While conventional CD3+ WT31+ cells produced IL 2 in response to mAb directed to CD2, CD3 or T44 surface molecules, CD3+ WT31- cells did not respond to anti-T44 mAb but released IL 2 following stimulation with anti-CD2 or anti-CD3 mAb. Therefore, assuming that anti-T44 mimicks the effect of a still undefined natural ligand our data suggest that T cells expressing the γ-gene surface product may be signalled by stimuli which differ, at least in part, from those acting on CD3+ WT31+ T lymphocytes.",
author = "A. Poggi and C. Bottino and Zocchi, {M. R.} and G. Pantaleo and E. Ciccone and C. Mingari and L. Moretta and A. Moretta",
year = "1987",
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TY - JOUR

T1 - CD3+ WT31- peripheral T lymphocytes lack T44 (CD28), a surface molecule involved in activation of T cells bearing the α/β heterodimer

AU - Poggi, A.

AU - Bottino, C.

AU - Zocchi, M. R.

AU - Pantaleo, G.

AU - Ciccone, E.

AU - Mingari, C.

AU - Moretta, L.

AU - Moretta, A.

PY - 1987

Y1 - 1987

N2 - We have applied two-color fluorescence cytofluorometric techniques to the analysis of the distribution of T44 and CD3 antigens in peripheral blood human lymphocytes. While most CD3+ cells co-expressed T44 antigen, a small distinct subset was CD3+ T44- (2-10% of CD3+ cells). This cell subset also did not react with the WT31 monoclonal antibody (mAb), specific for an α/β framework determinant of the T cell receptor (TCR). Lack of T44 antigen expression was also observed in purified CD3+ WT31- polyclonal populations that had been cultured in medium containing interleukin 2 (IL 2) and as well as >30 clones expressing the CD3+4-8-WT31- surface phenotype. Immunoprecipitation experiments confirmed that expression of T44 molecules was confined to CD3+ WT31+ peripheral blood T cells. While conventional CD3+ WT31+ cells produced IL 2 in response to mAb directed to CD2, CD3 or T44 surface molecules, CD3+ WT31- cells did not respond to anti-T44 mAb but released IL 2 following stimulation with anti-CD2 or anti-CD3 mAb. Therefore, assuming that anti-T44 mimicks the effect of a still undefined natural ligand our data suggest that T cells expressing the γ-gene surface product may be signalled by stimuli which differ, at least in part, from those acting on CD3+ WT31+ T lymphocytes.

AB - We have applied two-color fluorescence cytofluorometric techniques to the analysis of the distribution of T44 and CD3 antigens in peripheral blood human lymphocytes. While most CD3+ cells co-expressed T44 antigen, a small distinct subset was CD3+ T44- (2-10% of CD3+ cells). This cell subset also did not react with the WT31 monoclonal antibody (mAb), specific for an α/β framework determinant of the T cell receptor (TCR). Lack of T44 antigen expression was also observed in purified CD3+ WT31- polyclonal populations that had been cultured in medium containing interleukin 2 (IL 2) and as well as >30 clones expressing the CD3+4-8-WT31- surface phenotype. Immunoprecipitation experiments confirmed that expression of T44 molecules was confined to CD3+ WT31+ peripheral blood T cells. While conventional CD3+ WT31+ cells produced IL 2 in response to mAb directed to CD2, CD3 or T44 surface molecules, CD3+ WT31- cells did not respond to anti-T44 mAb but released IL 2 following stimulation with anti-CD2 or anti-CD3 mAb. Therefore, assuming that anti-T44 mimicks the effect of a still undefined natural ligand our data suggest that T cells expressing the γ-gene surface product may be signalled by stimuli which differ, at least in part, from those acting on CD3+ WT31+ T lymphocytes.

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