The JI
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     
 

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sleckman, B. P.
Right arrow Articles by Greenstein, J. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sleckman, B. P.
Right arrow Articles by Greenstein, J. L.

The Journal of Immunology, Vol 141, Issue 1 49-54, Copyright © 1988 by American Association of Immunologists

ARTICLES

Functional analysis of a cytoplasmic domain-deleted mutant of the CD4 molecule

BP Sleckman, A Peterson, JA Foran, JC Gorga, CJ Kara, JL Strominger, SJ Burakoff and JL Greenstein
Division of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA.

The CD4 molecule is a receptor found on a subset of T lymphocytes. It has been proposed that, upon binding MHC class II molecules expressed on APC, the CD4 molecule enhances the responsiveness of the T cell by increasing intercellular avidity and/or by transducing an intracellular signal. We have analyzed the effect of removing the cytoplasmic domain of the CD4 molecule on the ability of the CD4 molecule to enhance T cell responsiveness. The cytoplasmic domain-deleted mutant of the CD4 molecule (CD4 delta) was found to be as efficient as the CD4 molecule at enhancing responsiveness to cells bearing the appropriate Ag. If subcellular Ag in the form of purified Ag incorporated into liposomes was used, the CD4 molecule was found to be much more efficient than the CD4 delta molecule at enhancing responsiveness. However, the defect in the ability of the CD4 delta molecule to enhance responsiveness could be compensated for by increasing the level of expression of the CD4 delta molecule.


This article has been cited by other articles:


Home page
 J. Immunol.Home page
J. Zhang, K. Salojin, and T. L. Delovitch
Sequestration of CD4-Associated Lck from the TCR Complex May Elicit T Cell Hyporesponsiveness in Nonobese Diabetic Mice
J. Immunol., February 1, 1998; 160(3): 1148 - 1157.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1988 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1988 by The American Association of Immunologists, Inc. All rights reserved.