Immunopathogenesis of ischemia/reperfusion-associated tissue damage
Copyright © 2011 Elsevier Inc. All rights reserved.
| Publié dans: | Clinical immunology (Orlando, Fla.). - 1999. - 141(2011), 1 vom: 15. Okt., Seite 3-14 |
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| Auteur principal: | |
| Autres auteurs: | , |
| Format: | Article en ligne |
| Langue: | English |
| Publié: |
2011
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| Accès à la collection: | Clinical immunology (Orlando, Fla.) |
| Sujets: | Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Review Autoantibodies Toll-Like Receptors Complement System Proteins 9007-36-7 |
| Résumé: | Copyright © 2011 Elsevier Inc. All rights reserved. Ischemia/reperfusion (IR) instigates a complex array of inflammatory events which result in damage to the local tissue. IR-related organ damage occurs invariably in several clinical conditions including trauma, organ transplantation, autoimmune diseases and revascularization procedures. We critically review available pre-clinical experimental information on the role of immune response in the expression of tissue damage following IR. Distinct elements of the innate and adaptive immune response are involved in the expression of tissue injury. Interventions such as prevention of binding of natural antibody to antigen expressed on the surface of ischemia-conditioned cells, inhibition of the ensuing complement activation, modulation of Toll-like receptors, B or T cell depletion and blockade of inflammatory cytokines and chemokines limit IR injury in preclinical studies. Clinical trials that will determine the therapeutic value of each approach is needed |
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| Description: | Date Completed 21.11.2011 Date Revised 29.09.2011 published: Print-Electronic Citation Status MEDLINE |
| ISSN: | 1521-7035 |
| DOI: | 10.1016/j.clim.2011.07.001 |