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
Right arrow Citation Map
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
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bell, G. M.
Right arrow Articles by Imboden, J. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bell, G. M.
Right arrow Articles by Imboden, J. B.

The Journal of Immunology, Vol 151, Issue 7 3646-3653, Copyright © 1993 by American Association of Immunologists


ARTICLES

CD45-negative mutants of a rat natural killer cell line fail to lyse tumor target cells

GM Bell, GM Dethloff and JB Imboden
Department of Medicine, San Francisco VA Medical Center, CA.

To examine the role of CD45 in NK cell activation, we isolated three mutants and one variant of a rat NK cell line, RNK-16. Each of these lacked cell-surface expression of CD45 and did not have detectable transcripts for CD45 on Northern blot analysis. The CD45-negative cells expressed CD2, CD53, and NKR-P1, but mAb-induced perturbations of these molecules did not induce protein tyrosine phosphorylations and increases in the concentration of cytoplasmic-free calcium, as occurred in the wild-type RNK-16. Unlike the wild-type cells, the CD45-negative cells failed to lyse YAC-1 and RL-male-1 tumor targets. The cytolytic activity of the CD45-negative cells could be stimulated pharmacologically by ionomycin and PMA, which, when added to the cytotoxicity assays, induced killing of tumor targets. These studies suggest that CD45 is required for the response of RNK-16 cells to target cells and for signaling through CD2, CD53, and NKR-P1.


This article has been cited by other articles:


Home page
J. Immunol.Home page
L. H. Mason, J. Willette-Brown, L. S. Taylor, and D. W. McVicar
Regulation of Ly49D/DAP12 Signal Transduction by Src-Family Kinases and CD45.
J. Immunol., June 1, 2006; 176(11): 6615 - 6623.
[Abstract] [Full Text] [PDF]


Home page
JEMHome page
N. D. Huntington, Y. Xu, S. L. Nutt, and D. M. Tarlinton
A requirement for CD45 distinguishes Ly49D-mediated cytokine and chemokine production from killing in primary natural killer cells
J. Exp. Med., May 2, 2005; 201(9): 1421 - 1433.
[Abstract] [Full Text] [PDF]


Home page
Int ImmunolHome page
K. L. Puls, K. A. Hogquist, N. Reilly, and M. D. Wright
CD53, a thymocyte selection marker whose induction requires a lower affinity TCR-MHC interaction than CD69, but is up-regulated with slower kinetics
Int. Immunol., March 1, 2002; 14(3): 249 - 258.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
K. M. Giezeman-Smits, A. Gorter, R. L. P. van Vlierberghe, J. D. H. v. Eendenburg, A. M. M. Eggermont, G. J. Fleuren, and P. J. K. Kuppen
The Regulatory Role of CD45 on Rat NK Cells in Target Cell Lysis
J. Immunol., July 1, 1999; 163(1): 71 - 76.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
K. Kitamura, A. Maiti, D. H. W. Ng, P. Johnson, A. L. Maizel, and A. Takeda
Characterization of the Interaction between CD45 and CD45-AP
J. Biol. Chem., September 8, 1995; 270(36): 21151 - 21157.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1993 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1993 by The American Association of Immunologists, Inc. All rights reserved.