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Humoral Immune Responses

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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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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...

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Drug-related allergies are immune-mediated responses triggered by the administration of pharmacological agents. These hypersensitivity reactions are classified based on the immune mechanisms involved. The four primary types—Type I, II, III, and IV—are mediated by different immunological pathways and exhibit distinct clinical manifestations.Type I Hypersensitivity/ IgE-Mediated Reactions: Immunoglobulin E (IgE) immediately mediates Type I hypersensitivity reactions. Upon initial exposure to a...

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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...

Hypersensitivity Reactions: Immune-Complex Reactions

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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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Granulocyte-dependent Autoantibody-induced Skin Blistering

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Hypocomplementemia in chronic idiopathic urticaria

D A Mathison, C M Arroyave, K N Bhat

Annals of Internal Medicine

|May 1, 1977

Summary

This summary is machine-generated.

Chronic urticaria may stem from immune vasculitis and hypocomplementemia. This study found complement activation pathways in patients with chronic urticaria, suggesting new diagnostic clues.

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Area of Science:

Immunology
Dermatology
Pathophysiology

Background:

Chronic urticaria (CU) and angioedema often lack identifiable triggers or mechanisms.
Immune cutaneous vasculitis is a potential, though infrequently recognized, cause of CU.

Observation:

Two cases presented chronic urticaria as the primary symptom of immune cutaneous vasculitis.
Hypocomplementemia was observed in these cases, linked to complement activation via classic and alternative pathways.

Findings:

Among 72 CU patients, 10 with idiopathic urticaria showed hypocomplementemia.
These 10 patients exhibited varying patterns of complement pathway activation (classic, alternative, or both).
Circulating immune complexes were prevalent in patients with classic pathway activation.

Implications:

Hypocomplementemia may serve as a diagnostic indicator for specific pathophysiologic mechanisms in some CU patients.
Identifying complement activation pathways could refine understanding and management of chronic urticaria.
This research highlights the role of immune dysregulation in chronic urticarial conditions.