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      Identification of the target self-antigens in reperfusion injury

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          Abstract

          Reperfusion injury (RI), a potential life-threatening disorder, represents an acute inflammatory response after periods of ischemia resulting from myocardial infarction, stroke, surgery, or trauma. The recent identification of a monoclonal natural IgM that initiates RI led to the identification of nonmuscle myosin heavy chain type II A and C as the self-targets in two different tissues. These results identify a novel pathway in which the innate response to a highly conserved self-antigen expressed as a result of hypoxic stress results in tissue destruction.

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          Inferences, questions and possibilities in Toll-like receptor signalling.

          Bruce Beutler (2004)
          The Toll-like receptors (TLRs) are the key proteins that allow mammals--whether immunologically naive or experienced--to detect microbes. They lie at the core of our inherited resistance to disease, initiating most of the phenomena that occur in the course of infection. Quasi-infectious stimuli that have been used for decades to study inflammatory mechanisms can activate the TLR family of proteins. And it now seems that many inflammatory processes, both sterile and infectious, may depend on TLR signalling. We are in a good position to apply our understanding of TLR signalling to a range of challenges in immunology and medicine.
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            Intestinal mucosal lesion in low-flow states. I. A morphological, hemodynamic, and metabolic reappraisal.

            C. J. Chiu, A McArdle, R. Brown … (1970)
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              Reactive species mechanisms of cellular hypoxia-reoxygenation injury.

              Chuanyu Li, Robert M Jackson (2002)
              Exacerbation of hypoxic injury after restoration of oxygenation (reoxygenation) is an important mechanism of cellular injury in transplantation and in myocardial, hepatic, intestinal, cerebral, renal, and other ischemic syndromes. Cellular hypoxia and reoxygenation are two essential elements of ischemia-reperfusion injury. Activated neutrophils contribute to vascular reperfusion injury, yet posthypoxic cellular injury occurs in the absence of inflammatory cells through mechanisms involving reactive oxygen (ROS) or nitrogen species (RNS). Xanthine oxidase (XO) produces ROS in some reoxygenated cells, but other intracellular sources of ROS are abundant, and XO is not required for reoxygenation injury. Hypoxic or reoxygenated mitochondria may produce excess superoxide (O) and release H(2)O(2), a diffusible long-lived oxidant that can activate signaling pathways or react vicinally with proteins and lipid membranes. This review focuses on the specific roles of ROS and RNS in the cellular response to hypoxia and subsequent cytolytic injury during reoxygenation.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Exp Med
                Title: The Journal of Experimental Medicine
                Publisher: The Rockefeller University Press
                ISSN (Print): 0022-1007
                ISSN (Electronic): 1540-9538
                Publication date (Print): 23 January 2006
                Volume: 203
                Issue: 1
                Pages: 141-152
                Affiliations
                [1 ]CBR Institute for Biomedical Research, Inc., [2 ]Department of Pathology, [3 ]Department of Surgery, [4 ]Department of Pediatrics, and [5 ]Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115
                [6 ]Center for Molecular Imaging Research, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129
                [7 ]DecImmune Therapeutics, Boston, MA 02115
                Author notes

                CORRESPONDENCE Michael C. Carroll: carroll@ 123456cbr.med.harvard.edu

                Article
                Publisher ID: 20050390
                DOI: 10.1084/jem.20050390
                PMC ID: 2118091
                PubMed ID: 16390934
                SO-VID: 9c07400a-8743-4a77-b184-33e82a6cad26
                Copyright © Copyright © 2006, The Rockefeller University Press
                History
                Date received : 22 February 2005
                Date accepted : 2 December 2005
                Categories
                Subject: Articles
                Subject: Article

                ScienceOpen disciplines: Medicine
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                ScienceOpen disciplines: Medicine

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