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Interdependence of CD3‐Ti and CD2 activation pathways in human T lymphocytes.
Author(s) -
Alcover A.,
Alberini C.,
Acuto O.,
Clayton L. K.,
Transy C.,
Spagnoli G. C.,
Moingeon P.,
Lopez P.,
Reinherz E. L.
Publication year - 1988
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1988.tb03035.x
Subject(s) - cancer , biology , library science , computer science , genetics
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.