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Human T lymphocytes can be activated through either the antigen/MHC receptor complex T3-Ti (CD3-Ti) or the T11 (CD2) molecule to proliferate via an IL-2 dependent mechanism. To investigate the relationship of these pathways to one another, we generated and characterized Jurkat mutants which selectively express either surface CD3-Ti or CD2. Here we show that CD3-Ti- mutants fail to be stimulated by either pathway to increase phosphoinositide turnover, mobilize calcium or induce the IL-2 gene. The activation capacity of these mutants via CD2 as well as CD3-Ti can be restored following reconstitution of surface CD3-Ti expression upon appropriate DNA transfer (e.g. Ti beta subunit cDNA into Ti beta- Jurkat variants). Collectively, these results demonstrate that CD3-Ti and CD2 pathways are interdependent and that phosphoinositide turnover is linked to the CD3-Ti complex.


Journal article



Publication Date





1973 - 1977


Antigens, Differentiation, Antigens, Differentiation, T-Lymphocyte, CD2 Antigens, CD3 Complex, Calcium, Genes, Humans, Inositol, Interleukin-2, Lymphocyte Activation, Lymphocyte Function-Associated Antigen-1, Major Histocompatibility Complex, Receptors, Antigen, T-Cell, Receptors, Immunologic, T-Lymphocytes, Transcription, Genetic