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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...

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Related Experiment Video

Updated: Jul 14, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

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Published on: October 12, 2012

Acute immunologic arthritis in rabbits.

C V DeShazo, P M Henson, C G Cochrane

    The Journal of Clinical Investigation
    |January 1, 1972
    PubMed
    Summary

    Neutrophils and complement are key to acute immunologic joint injury. Complement component 6 (C6) and C3 are crucial for vascular permeability and neutrophil accumulation in arthritic rabbit knees.

    Area of Science:

    • Immunology
    • Pathology
    • Rheumatology

    Background:

    • Acute immunologic injury, such as arthritis, involves complex inflammatory processes.
    • Understanding the roles of immune cells and complement in joint inflammation is critical for developing targeted therapies.

    Purpose of the Study:

    • To investigate the in vivo mediators of acute immunologic injury in a rabbit arthritis model.
    • To elucidate the specific roles of neutrophils and complement components (C3, C6) in the development of synovial lesions.

    Main Methods:

    • A reversed passive Arthus lesion was induced in rabbit knee joints via antibody and antigen injection.
    • Vascular permeability and neutrophil accumulation were quantified by measuring protein leakage and cell counts.
    • Complement-deficient rabbits (C6, C3) and neutrophil-depleted rabbits were utilized to assess mediator function.

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    Main Results:

    • Two distinct peaks of vascular permeability correlated with neutrophil accumulation, indicating their central role.
    • Neutrophil depletion abrogated the lesion, while reconstitution with neutrophils restored it.
    • Complement deficiency (C6, C3) significantly delayed or reduced vascular permeability, neutrophil influx, and lesion development.

    Conclusions:

    • Neutrophils are essential effectors of acute immunologic injury in the synovial joint.
    • Complement, particularly C6 and C3, plays a critical role in initiating and amplifying the inflammatory cascade, including neutrophil recruitment.
    • Antigen-antibody-complement complexes directly attract neutrophils, highlighting their importance in initiating the inflammatory response.