HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Greenberg, P. D. Articles by Bluestein, H. G. Search for Related Content PubMed Articles by Greenberg, P. D. Articles by Bluestein, H. G.

Antigen Recognition by Primed T Lymphocytes in Vitro

I. Separation of Recognitive and Proliferative Phases of Antigen-Induced T Cell Activation¹

From the Department of Medicine, University of California Medical Center, San Diego, California 92103

Abstract

Antigen-induced T cell activation can be separated into early recognitive events and later proliferative events. After in vitro challenge of primed lymphocytes with antigen, enhanced transmembrane transport of -aminoisobutyric acid (¹⁴C-AIB), a nonutilizable amino acid, can be demonstrated within 4 to 8 hr, and is at or near maximum by 8 to 16 hr of culture. The response is antigen specific and requires that the primed animal is a genetic responder to the immunizing antigen. Therefore, AIB uptake was utilized as a probe of antigen recognition and compared to tritiated thymidine incorporation, a measure of DNA synthesis. Colchicine, cytochalasin B, and Ca⁺⁺ depletion have been reported to block DNA synthesis in activated lymphocytes and to interfere with macrophage-T cell interaction. We confirmed that these agents effectively abrogated antigen-induced DNA synthesis under conditions which, in contrast, had little effect on antigen-induced AIB uptake. We interpret these results to indicate at least a two-signal model for antigen-induced T cell proliferation. An initial signal is generated by the interaction of antigen with its membrane receptor. Lymphocyte activation commences but at some step before the initiation of S-phase, a second critical event, which can be blocked by colchicine, cytochalasin B, and Ca⁺⁺ depletion, must occur. Since those agents block macrophage-T cell binding, the second signal may be the result of that cell-cell binding.

Footnotes

¹ This work was supported by Grant AI-10931 from the National Institute of Allergy and Infectious Diseases.

² Recipient of Research Fellowship AI-02134 from the National Institute of Allergy and Infectious Diseases.