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PMID: 3309950 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

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

Goldsmith MA, Weiss A

Abstract

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.

MeSH Terms
Antigens, Differentiation, T-Lymphocyte/analysis Calcium/metabolism Cell Line Flow Cytometry Fluorescent Antibody Technique Humans Inositol Phosphates/metabolism Mutation Receptors, Antigen, T-Cell/immunology T-Lymphocytes/immunology,metabolism
Chemicals
Antigens, Differentiation, T-Lymphocyte Inositol Phosphates Receptors, Antigen, T-Cell Calcium
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Goldsmith M A
Howard Hughes Medical Institute, Department of Medicine, University of California, San Francisco 94143.
Weiss A
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18 references, click to expand
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Article Info
Journal
Proceedings of the National Academy of Sciences of the United States of America
Abbr.
Proc Natl Acad Sci U S A
ISSN
0027-8424
Published
1987-10-00
Pages
6879-83
Language
English
Region
United States
NLM ID
7505876
PMCID
PMC299188
Subset
IM
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