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Related Concept Videos

Allergic Drug Reactions01:27

Allergic Drug Reactions

Allergic reactions related to drugs are hypersensitivity responses driven by the immune system and bear no connection to the drug's therapeutic action. While drugs in isolation do not trigger an immune response, they can interact with endogenous proteins to form antigens. These antigens stimulate lymphocytes to produce antibodies. IgE-type antibodies attach themselves to mast cells. Upon subsequent exposure to the same stimulus, the antigen-antibody interaction is initiated, unleashing numerous...
Drug Toxicity: Allergic Reactions01:30

Drug Toxicity: Allergic Reactions

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...
Allergic Reactions: Anaphylaxis01:30

Allergic Reactions: Anaphylaxis

Anaphylaxis is a severe, life-threatening hypersensitivity reaction mediated by Immunoglobulin E (IgE) antibodies. When IgE binds to allergens, it triggers the release of mediators– histamine, leukotrienes, and prostaglandins from mast cells and basophils. These mediators cause vasodilation, edema, and inflammation, leading to various symptoms.The primary allergens causing anaphylaxis include food items (e.g., peanuts, shellfish), drugs (e.g., penicillin, asparaginase, corticotropin, heparin),...
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...
Hypersensitivity Reactions: Delayed Hypersensitivity Reactions01:29

Hypersensitivity Reactions: Delayed Hypersensitivity Reactions

Delayed-Type Hypersensitivity (DTH), or Type IV hypersensitivity, is a cell-mediated immune response. It occurs when T cells, rather than antibodies, mediate a reaction to specific antigens. It is characterized by a delayed onset (1-2 days) and involves the recruitment of macrophages to the inflammation site.The initiation of a DTH response begins with the sensitization of T cells. During this phase, which lasts at least 1-2 weeks, antigen-specific T cells are activated, clonally expanded, and...
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 5, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

HLA antigens and corticosteroid response.

B Becker, D H Shin, P F Palmberg

    Science (New York, N.Y.)
    |December 24, 1976
    PubMed
    Summary

    Patients with primary open-angle glaucoma show higher rates of specific HLA antigens and increased sensitivity to glucocorticoids. Their lymphocytes require lower prednisolone doses to inhibit transformation, suggesting a link between immune response and glaucoma.

    Area of Science:

    • Immunogenetics
    • Ophthalmology

    Background:

    • Primary open-angle glaucoma (POAG) is associated with specific human leukocyte antigen (HLA) types.
    • Glaucoma patients exhibit altered responses to glucocorticoids.

    Purpose of the Study:

    • To investigate the association between HLA antigens and glucocorticoid responsiveness in POAG patients.
    • To determine if HLA-B12 antigen influences lymphocyte sensitivity to prednisolone in ocular normotensive and glaucomatous individuals.

    Main Methods:

    • Comparison of HLA antigen prevalence in POAG patients versus normal individuals.
    • Assessment of lymphocyte transformation response to phytohemagglutinin.
    • Quantification of prednisolone concentrations required to inhibit lymphocyte transformation.

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    Personalized Peptide Arrays for Detection of HLA Alloantibodies in Organ Transplantation
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    Personalized Peptide Arrays for Detection of HLA Alloantibodies in Organ Transplantation

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    Last Updated: Jul 5, 2026

    Granulocyte-dependent Autoantibody-induced Skin Blistering
    12:23

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    Published on: October 12, 2012

    Anti-Nuclear Antibody Screening Using HEp-2 Cells
    13:01

    Anti-Nuclear Antibody Screening Using HEp-2 Cells

    Published on: June 24, 2014

    Personalized Peptide Arrays for Detection of HLA Alloantibodies in Organ Transplantation
    08:07

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    Published on: September 6, 2017

    Main Results:

    • Increased prevalence of HLA-B12 and B7 antigens in POAG patients.
    • Lymphocytes from individuals with HLA-B12 antigen (both ocular normotensive and glaucomatous) showed significantly lower prednisolone concentrations required for inhibiting phytohemagglutinin-induced transformation (P < .02).

    Conclusions:

    • The HLA-B12 antigen is linked to increased glucocorticoid responsiveness in lymphocytes.
    • This heightened sensitivity may play a role in the pathogenesis or progression of primary open-angle glaucoma.