The JI PBL Intereron Source
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Reiter, Y.
Right arrow Articles by Fishelson, Z.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Reiter, Y.
Right arrow Articles by Fishelson, Z.

The Journal of Immunology, Vol 155, Issue 4 2203-2210, Copyright © 1995 by American Association of Immunologists

ARTICLES

Complement membrane attack complex, perforin, and bacterial exotoxins induce in K562 cells calcium-dependent cross-protection from lysis

Y Reiter, A Ciobotariu, J Jones, BP Morgan and Z Fishelson
Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel.

The complement membrane attack complex (MAC), the cytolytic granule protein of cytotoxic lymphocytes perforin, the streptococcal exotoxin streptolysin O (SLO), and the bee venom polypeptide melittin utilize a similar mechanism to incorporate into cell membranes, induce a Ca2+ influx and a rise in intracellular Ca2+ concentration, and produce cell lysis. At sublytic concentrations, these proteins trigger several cellular activities, including protein phosphorylation and synthesis. We have recently demonstrated that human leukemic cells treated with sublytic doses of human complement become more resistant to lytic complement doses. The study has now been extended to include three other pore-formers: murine perforin, SLO and melittin. As shown here, sublytic MAC induces in the K562 human erythroleukemic cells protection from lytic perforin, and vice versa, sublytic perforin induces protection from complement. Also, sublytic SLO and melittin increase resistance of K562 cells to lytic complement and perforin doses. The capacity of Ca2+ ionophores to induce resistance to the lytic proteins has been examined. Exposure of K562 cells to sublytic concentrations of ionomycin or A23187 for 1 h at 37 degrees C confers on them resistance to complement- and perforin-mediated lysis. The protective effects of the ionophores can be abrogated by chelation of extracellular Ca2+ and by inhibition of RNA or protein synthesis in the cells. These results indicate the following: 1) nucleated cells exposed to sublytic complement MAC, perforin, SLO, or melittin may become resistant to the four pore-formers. Physiologically, this may be regarded as an immunologic tachyphylaxis. 2) Ca2+ influx induced by these pore-formers is an essential and sufficient factor to produce this tachyphylaxis.


This article has been cited by other articles:


Home page
 J. Immunol.Home page
L. Ziporen, N. Donin, T. Shmushkovich, A. Gross, and Z. Fishelson
Programmed Necrotic Cell Death Induced by Complement Involves a Bid-Dependent Pathway
J. Immunol., January 1, 2009; 182(1): 515 - 521.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
P. V. Beum, M. A. Lindorfer, F. Beurskens, P. T. Stukenberg, H. M. Lokhorst, A. W. Pawluczkowycz, P. W. H. I. Parren, J. G. J. van de Winkel, and R. P. Taylor
Complement Activation on B Lymphocytes Opsonized with Rituximab or Ofatumumab Produces Substantial Changes in Membrane Structure Preceding Cell Lysis
J. Immunol., July 1, 2008; 181(1): 822 - 832.
[Abstract] [Full Text] [PDF]

Home page
 Infect. Immun.Home page
N. O. Gekara, L. Groebe, N. Viegas, and S. Weiss
Listeria monocytogenes Desensitizes Immune Cells to Subsequent Ca2+ Signaling via Listeriolysin O-Induced Depletion of Intracellular Ca2+ Stores
Infect. Immun., February 1, 2008; 76(2): 857 - 862.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
O. Moskovich and Z. Fishelson
Live Cell Imaging of Outward and Inward Vesiculation Induced by the Complement C5b-9 Complex
J. Biol. Chem., October 12, 2007; 282(41): 29977 - 29986.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
E. A. Booth and B. R. Lucchesi
Medroxyprogesterone acetate prevents the cardioprotective and anti-inflammatory effects of 17beta-estradiol in an in vivo model of myocardial ischemia and reperfusion
Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1408 - H1415.
[Abstract] [Full Text] [PDF]

Home page
 Molecular Cancer TherapeuticsHome page
W. S. Yang, S.-O Park, A-R. Yoon, J. Y. Yoo, M. K. Kim, C.-O. Yun, and C.-W. Kim
Suicide cancer gene therapy using pore-forming toxin, streptolysin O.
Mol. Cancer Ther., June 1, 2006; 5(6): 1610 - 1619.
[Abstract] [Full Text] [PDF]

Home page
 Int ImmunolHome page
D. Pilzer and Z. Fishelson
Mortalin/GRP75 promotes release of membrane vesicles from immune attacked cells and protection from complement-mediated lysis
Int. Immunol., September 1, 2005; 17(9): 1239 - 1248.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
A. P. Dalmasso, B. A. Benson, J. S. Johnson, C. Lancto, and M. S. Abrahamsen
Resistance Against the Membrane Attack Complex of Complement Induced in Porcine Endothelial Cells with a Gal{alpha}(1-3)Gal Binding Lectin: Up-Regulation of CD59 Expression
J. Immunol., April 1, 2000; 164(7): 3764 - 3773.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1995 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1995 by The American Association of Immunologists, Inc. All rights reserved.