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Related Concept Videos

Inflammation01:38

Inflammation

Overview
Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
Hypersensitivity Reactions: Cytolytic Reactions01:01

Hypersensitivity Reactions: Cytolytic Reactions

Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...
Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum sickness, a systemic...

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Related Experiment Video

Updated: Jul 18, 2026

A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion
13:42

A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion

Published on: July 17, 2012

Ischaemia-reperfusion is an event triggered by immune complexes and complement.

R K Chan1, S I Ibrahim, N Verna

  • 1Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. hhechtman@partners.org

The British Journal of Surgery
|December 4, 2003
PubMed
Summary

Reperfusion injury, a clinical challenge, may be driven by immune responses rather than free radicals. New evidence highlights complement activation and immune complexes as key mediators.

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Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy
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A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion
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Inducing Ischemia-reperfusion Injury in the Mouse Ear Skin for Intravital Multiphoton Imaging of Immune Responses
06:29

Inducing Ischemia-reperfusion Injury in the Mouse Ear Skin for Intravital Multiphoton Imaging of Immune Responses

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Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy
07:05

Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy

Published on: September 27, 2024

Area of Science:

  • Immunology
  • Pathophysiology
  • Medical Science

Background:

  • Reperfusion injury presents a significant clinical challenge with limited therapeutic options.
  • Previous research focusing on oxygen free radicals and neutrophils has yielded no successful clinical treatments.
  • Understanding the underlying mechanisms of reperfusion injury is crucial for developing effective therapies.

Purpose of the Study:

  • To review recent clinical and preclinical findings on mitigating reperfusion injury.
  • To identify novel therapeutic targets and strategies for managing reperfusion injury.
  • To synthesize current evidence on the pathophysiology of reperfusion injury.

Main Methods:

  • Comprehensive literature review of MEDLINE database (1966-2003).
  • Inclusion of studies without language restrictions.
  • Analysis of both clinical and preclinical data on reperfusion injury.

Main Results:

  • Emerging evidence implicates the complement system and immune complexes in reperfusion injury.
  • Ischemia may induce cellular changes, leading to neoantigen expression.
  • Natural IgM antibodies can be trapped, initiating complement activation.

Conclusions:

  • Complement activation and immune complexes are critical in mediating reperfusion injury.
  • Formation of the membrane attack complex and mast cell degranulation are key terminal events.
  • This understanding offers new avenues for therapeutic intervention in reperfusion injury.