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Related Concept Videos

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...
Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
Inflammatory Response01:28

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An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
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Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Hypersensitivities01:30

Hypersensitivities

Hypersensitivity, also known as a hypersensitivity reaction or allergic reaction, is a condition where the body's immune system reacts abnormally to a foreign substance. Such substances, that cause hypersensitivity are referred to as an allergen, could be something typically harmless to most people, like pollen or certain foods.
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Acute Inflammation I: Inflammatory Response01:26

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Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated...

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Updated: Jun 26, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering
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Published on: October 12, 2012

Compensatory anti-inflammatory response syndrome.

Minou Adib-Conquy1, Jean-Marc Cavaillon

  • 1Unit Cytokines & Inflammation, Institut Pasteur, 28 rue Dr. Roux, 75015 Paris, France. madib@pasteur.fr

Thrombosis and Haemostasis
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Summary

Compensatory anti-inflammatory response syndrome (CARS) explains immune changes after critical illness, potentially increasing infection risk. It involves leukocyte reprogramming, not a global immune defect, aiding localized anti-inflammatory responses.

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Area of Science:

  • Immunology
  • Critical Care Medicine
  • Pathophysiology

Background:

  • Compensatory anti-inflammatory response syndrome (CARS) was proposed to explain immune counter-regulation following severe inflammation (SIRS) or sepsis.
  • CARS can lead to altered immune status, increasing susceptibility to nosocomial infections in critically ill patients.
  • Animal models suggest enhanced infection sensitivity after initial insults, though this is experimentally variable.

Purpose of the Study:

  • To explore the concept of CARS and its impact on immune function.
  • To investigate the reprogramming of leukocyte functions in sepsis and SIRS.
  • To understand the localized tissue response in CARS.

Main Methods:

  • Review of existing literature on CARS, sepsis, and SIRS.
  • Analysis of immune cell function alterations in patients and animal models.
  • Examination of gene expression patterns in leukocytes.

Main Results:

  • CARS involves a reprogramming of circulating leukocytes rather than a global defect in immune cell function.
  • Leukocytes within tissues appear primed or activated, not globally immunosuppressed.
  • The immune response in CARS is compartmentalized, silencing some inflammatory genes while maintaining anti-infectious gene expression.

Conclusions:

  • CARS represents an adapted, compartmentalized immune response to control excessive inflammation.
  • It balances the silencing of pro-inflammatory genes with the maintenance of anti-infectious defenses.
  • Understanding CARS is crucial for managing infection risk in critically ill patients.