| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
* Department of Cellular Injury, Walter Reed Army Institute of Research, Silver Spring, MD 20910;
Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD 20814;
Hospital for Special Surgery, New York, NY 10021;
Departments of Medicine and Immunology, University of Colorado Health Sciences Center, Denver, CO 80262; and
¶ Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, PA 19122
Complement receptor 2-deficient (Cr2–/–) mice are resistant to mesenteric ischemia/reperfusion (I/R) injury because they lack a component of the natural Ab repertoire. Neither the nature of the Abs that are involved in I/R injury nor the composition of the target Ag, to which recognition is lacking in Cr2–/– mice, is known. Because anti-phospholipid Abs have been shown to mediate fetal growth retardation and loss when injected into pregnant mice, we performed experiments to determine whether anti-phospholipid Abs can also reconstitute I/R injury and, therefore, represent members of the injury-inducing repertoire that is missing in Cr2–/– mice. We demonstrate that both murine and human monoclonal and polyclonal Abs against negatively charged phospholipids can reconstitute mesenteric I/R-induced intestinal and lung tissue damage in Cr2–/– mice. In addition, Abs against 
2 glycoprotein I restore local and remote tissue damage in the Cr2–/– mice. Unlike Cr2–/– mice, reconstitution of I/R tissue damage in the injury-resistant Rag-1–/– mouse required the infusion of both anti-2-glycoprotein I and anti-phospholipid Ab. We conclude that anti-phospholipid Abs can bind to tissues subjected to I/R insult and mediate tissue damage.
This article has been cited by other articles:
|
|
 |
|
  T. Moses, L. Wagner, and S. D. Fleming TLR4-mediated Cox-2 expression increases intestinal ischemia/reperfusion-induced damage J. Leukoc. Biol., October 1, 2009; 86(4): 971 - 980. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Kulik, S. D. Fleming, C. Moratz, J. W. Reuter, A. Novikov, K. Chen, K. A. Andrews, A. Markaryan, R. J. Quigg, G. J. Silverman, et al. Pathogenic Natural Antibodies Recognizing Annexin IV Are Required to Develop Intestinal Ischemia-Reperfusion Injury J. Immunol., May 1, 2009; 182(9): 5363 - 5373. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Shi, V. R. Moulton, P. H. Lapchak, G.-M. Deng, J. J. Dalle Lucca, and G. C. Tsokos Ischemia-mediated aggregation of the actin cytoskeleton is one of the major initial events resulting in ischemia-reperfusion injury Am J Physiol Gastrointest Liver Physiol, February 1, 2009; 296(2): G339 - G347. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. R. Kinderlerer, F. Ali, M. Johns, E. A. Lidington, V. Leung, J. J. Boyle, S. S. Hamdulay, P. C. Evans, D. O. Haskard, and J. C. Mason KLF2-dependent, Shear Stress-induced Expression of CD59: A NOVEL CYTOPROTECTIVE MECHANISM AGAINST COMPLEMENT-MEDIATED INJURY IN THE VASCULATURE J. Biol. Chem., May 23, 2008; 283(21): 14636 - 14644. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Lockshin and R. Derksen New developments in lupus-associated antiphospholipid syndrome Lupus, May 1, 2008; 17(5): 443 - 446. [Abstract] [PDF]
|
|
|
|
|
|
R. K. Chan, S. I. Ibrahim, K. Takahashi, E. Kwon, M. McCormack, A. Ezekowitz, M. C. Carroll, F. D. Moore Jr., and W. G. Austen Jr. The Differing Roles of the Classical and Mannose-Binding Lectin Complement Pathways in the Events following Skeletal Muscle Ischemia-Reperfusion J. Immunol., December 1, 2006; 177(11): 8080 - 8085. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Zhang, E. M. Alicot, I. Chiu, J. Li, N. Verna, T. Vorup-Jensen, B. Kessler, M. Shimaoka, R. Chan, D. Friend, et al. Identification of the target self-antigens in reperfusion injury J. Exp. Med., January 23, 2006; 203(1): 141 - 152. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Fischetti, P. Durigutto, V. Pellis, A. Debeus, P. Macor, R. Bulla, F. Bossi, F. Ziller, D. Sblattero, P. Meroni, et al. Thrombus formation induced by antibodies to {beta}2-glycoprotein I is complement dependent and requires a priming factor Blood, October 1, 2005; 106(7): 2340 - 2346. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
