Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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.

Type

Journal article

Journal

EMBO J

Publication Date

07/1988

Volume

7

Pages

1973 - 1977

Keywords

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