Isolation and characterization of a T-lymphocyte somatic mutant with altered signal transduction by the antigen receptor. | Zendy

Mark A. Goldsmith | Zendy; Arthur Weiss | Zendy

Open Access

Isolation and characterization of a T-lymphocyte somatic mutant with altered signal transduction by the antigen receptor.

Author(s) -

Mark A. Goldsmith,

Arthur Weiss

Publication year - 1987

Publication title -

proceedings of the national academy of sciences

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 5.011

H-Index - 771

eISSN - 1091-6490

pISSN - 0027-8424

DOI - 10.1073/pnas.84.19.6879

Subject(s) - signal transduction , biology , cd3 , mutant , antigen , microbiology and biotechnology , receptor , antibody , transduction (biophysics) , cell sorting , t cell receptor , t cell , immune system , biochemistry , immunology , flow cytometry , gene , cd8

We have developed an approach for deriving and characterizing antigen-receptor (CD3/Ti) signal-transduction mutants. This strategy combines receptor-mediated growth inhibition and fluorescence-activated cell sorting with the Ca2+-indicator indo-1. Despite the expression of structurally normal CD3/Ti complexes, one such mutant (J.CaM1) fails to exhibit inositolphospholipid metabolism or Ca2+ mobilization in response to anti-CD3 or anti-Ti monoclonal antibodies and fails to produce lymphokines in response to these antibodies. Surprisingly, anti-Ti antibody retains its effectiveness as a stimulus for the down-regulation of CD3/Ti surface expression. These cells remain responsive to AIF-4, at least one anti-CD3 antibody, and some combinations of nonagonist anti-Ti and anti-CD3 antibodies. The mutation in J.CaM1 appears to lie in a proximal component of the signal-transduction apparatus.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research