Characterization of CD3+, CD4-, CD8- clones expressing the putative T cell receptor γ gene product. Analysis of the activation pathways leading to interleukin 2 production and triggering of the lytic machinery

S. Ferrini, C. Bottino, R. Biassoni, A. Poggi, R. P. Sekaly, L. Moretta, A. Moretta

Research output: Contribution to journalArticlepeer-review

Abstract

Four clones were derived from human peripheral blood T lymphocytes from which CD4+ and CD8+ cells had been removed by treatment with specific mAbs and complement. All expressed the CD2+, 3+, 4-, 8-, T44- phenotype, and did not react with the WT31 mAb, which is specific for a framework determinant of the CD3-associated α/β heterodimer which serves as receptor for antigen on most human T lymphocytes. Surface iodination followed by crosslinking with dithiobis-succinimidyl propionate (DSP) and immunoprecipitation with anti-CD3 mAbs indicated that, in all four clones, the CD3-associated molecules consisted of a major 45 kD band and a minor band of 43 kD. Northern blot analysis showed that mRNA for the γ chain was expressed at high levels, whereas mRNA for the α chain was missing; β chain mRNA was present in a defective form (1 kb instead of 1.3 kb). These data support the concept that these clones may express, in association with CD3, the molecular product of the T cell receptor γ genes instead of the typical α/β heterodimer. CD3+, WT31- clones lysed the NK-sensitive K562 target cells and produced IL-2 upon stimulation with PHA. In addition, they released IL-2 after triggering with soluble anti-CD3 mAbs or with an appropriate combination of anti-CD2 mAbs (in the presence of adherent cells). When CD3+, WT31- clones were incubated with an anti-CD3 producing hybridoma as triggering target, the latter was efficiently lysed. Target cell lysis also occurred when a suitable combination of anti-CD2 mAbs-producing hybridomas was used. Therefore, CD3+, WT31- cells appear to use two pathways of cell activation that function also in conventional CD3+, WT31+ T cells, but they lack a third putative pathway initiated by T44 surface molecules.

Original languageEnglish
Pages (from-to)277-282
Number of pages6
JournalJournal of Experimental Medicine
Volume166
Issue number1
DOIs
Publication statusPublished - 1987

ASJC Scopus subject areas

  • Immunology

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