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 Collins, T.
Right arrow Articles by Pober, J. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Collins, T.
Right arrow Articles by Pober, J. S.

The Journal of Immunology, Vol 133, Issue 4 1878-1884, Copyright © 1984 by American Association of Immunologists

ARTICLES

Human cytolytic T lymphocyte interactions with vascular endothelium and fibroblasts: role of effector and target cell molecules

T Collins, AM Krensky, C Clayberger, W Fiers, MA Gimbrone Jr, SJ Burakoff and JS Pober

Monoclonal antibodies (mAb) against cell surface structures have been used to identify several molecules involved in the interaction of human cytolytic T lymphocytes (CTL) with lymphoid and other bone marrow- derived targets. In allograft rejection or in graft-vs-host disease, however, major cellular targets are vascular and stromal cells, especially endothelium. Yet little is known about whether the same cell surface molecules are involved in the interactions of CTL with these cell types. We assessed the ability of mAb against effector or target cell structures to inhibit cytolysis of susceptible, cultured human vascular endothelium or dermal fibroblasts by a cloned human CTL line. Using mAb reactive with T3, T4, LFA-1, LFA-2, LFA-3, and HLA-DR, we found a qualitatively similar but quantitatively different pattern of inhibition of cytolysis as previously established for lymphoid targets by using the same CTL clone. These results have two implications: 1) the target cell structures recognized by CTL molecules such as T4, LFA- 1 and LFA-2 are present on diverse cell types; and 2) the relative importance of such interactions may vary with target cell type. Furthermore, our studies provide several insights into the mechanisms of the interacting molecules. Our model system, and the use of pathophysiologically important target cells, may be useful for further analysis of CTL-mediated immune injury.


This article has been cited by other articles:


Home page
 J. Immunol.Home page
L. Zheng, T. J. Dengler, M. S. Kluger, L. A. Madge, J. S. Schechner, S. E. Maher, J. S. Pober, and A. L. M. Bothwell
Cytoprotection of Human Umbilical Vein Endothelial Cells Against Apoptosis and CTL-Mediated Lysis Provided by Caspase-Resistant Bcl-2 Without Alterations in Growth or Activation Responses
J. Immunol., May 1, 2000; 164(9): 4665 - 4671.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
C. Phan, A. W. McMahon, R. C. Nelson, J. F. Elliott, and A. G. Murray
Activated Lymphocytes Promote Endothelial Cell Detachment from Matrix: A Role for Modulation of Endothelial Cell {beta}1 Integrin Affinity
J. Immunol., October 15, 1999; 163(8): 4557 - 4563.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
K. Murakami, W. Ma, R. Fuleihan, and J. S. Pober
Human Endothelial Cells Augment Early CD40 Ligand Expression in Activated CD4+ T Cells Through LFA-3-Mediated Stabilization of mRNA
J. Immunol., September 1, 1999; 163(5): 2667 - 2673.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1984 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1984 by The American Association of Immunologists, Inc. All rights reserved.