Type II Hypersensitivity Quiz
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Questions and Answers

What is the consequence of antibodies binding to fixed tissue antigens in Type II hypersensitivity?

  • Activation of T cells and cellular immunity.
  • Phagocytosis of antigens by neutrophils.
  • Release of pro-inflammatory substances by neutrophils. (correct)
  • Stimulation of B cells to produce more antibodies.
  • Which mechanism is primarily involved in complement activation during Type II hypersensitivity?

  • Classical pathway. (correct)
  • Alternative pathway.
  • Lectin pathway.
  • Non-specific pathway.
  • In frustrated phagocytosis, neutrophils are unable to perform phagocytosis because they bind to IgG antibodies via which receptors?

  • Complement receptors.
  • Fc receptors. (correct)
  • Toll-like receptors.
  • Pattern recognition receptors.
  • What role does tissue damage play in the context of Type II hypersensitivity reactions?

    <p>It results from the release of reactive oxygen species and lysosomal enzymes.</p> Signup and view all the answers

    When antibodies are produced against red blood cell antigens, what is the primary result?

    <p>Destruction of the red blood cells.</p> Signup and view all the answers

    Which type of hypersensitivity reaction is primarily T cell-mediated?

    <p>Type IV hypersensitivity</p> Signup and view all the answers

    What are the antibodies involved in Type II hypersensitivity reactions?

    <p>IgG and IgM</p> Signup and view all the answers

    What is one consequence of complement activation in Type II hypersensitivity?

    <p>Release of inflammatory products</p> Signup and view all the answers

    Which of the following correctly describes Type III hypersensitivity?

    <p>Involves immune complex-mediated reactions</p> Signup and view all the answers

    What characteristic is unique to Type IV hypersensitivity compared to Types II and III?

    <p>It is predominantly a T cell-mediated response</p> Signup and view all the answers

    Which type of hypersensitivity reaction typically involves autoantibodies?

    <p>Type II hypersensitivity</p> Signup and view all the answers

    What plays a crucial role in the diagnosis of hypersensitivity reactions?

    <p>Skin tests</p> Signup and view all the answers

    In Type II hypersensitivity, what does the antigen react with on the cell surface?

    <p>Antibodies</p> Signup and view all the answers

    What primarily guides T cells to the site of infection?

    <p>Selectins and chemokine receptors</p> Signup and view all the answers

    What type of cells are primarily responsible for mediating Type IV hypersensitivity reactions?

    <p>Th1 cells</p> Signup and view all the answers

    What happens to CCR7 expression when T cells are activated?

    <p>It decreases</p> Signup and view all the answers

    Which cytokines play a significant role in recruiting T cells to the infection site?

    <p>C3a and C5a</p> Signup and view all the answers

    What cytokine is predominantly produced by Th1 cells to activate macrophages?

    <p>IFN-γ</p> Signup and view all the answers

    What is the primary consequence of autoimmune hemolytic anemia?

    <p>Decreased number of RBCs</p> Signup and view all the answers

    In Type III hypersensitivity, what triggers the complement activation?

    <p>Immune complexes depositing in blood vessels</p> Signup and view all the answers

    What is the typical time frame for the manifestation of delayed-type hypersensitivity reactions after antigen exposure?

    <p>24-48 hours</p> Signup and view all the answers

    What type of process allows T cells to move from blood vessels to tissues?

    <p>Rolling, adhesion, and transmigration</p> Signup and view all the answers

    Which type of immune complexes are primarily problematic in Type III hypersensitivity?

    <p>Small immune complexes</p> Signup and view all the answers

    How do activated macrophages improve their phagocytic ability?

    <p>By increasing Toll-like receptors expression</p> Signup and view all the answers

    What role do P-selectin, E-selectin, and L-selectin play in T cell migration?

    <p>They assist in T cell attachment to endothelia</p> Signup and view all the answers

    Which of the following T cell types is NOT involved in Type IV hypersensitivity?

    <p>Th2 cells</p> Signup and view all the answers

    What effect does increased vascular permeability have on T cell recruitment?

    <p>It allows edema and enhances T cell infiltration</p> Signup and view all the answers

    What results from the binding of antibodies specific for soluble antigens?

    <p>Formation of immune complexes</p> Signup and view all the answers

    What is the role of reactive oxygen species (ROS) produced by activated macrophages?

    <p>They enhance phagocytic activity</p> Signup and view all the answers

    What is one of the main consequences of the inflammation caused by Type III hypersensitivity?

    <p>Vasculitis</p> Signup and view all the answers

    Which receptor's expression increases in activated T cells to assist in their migration?

    <p>S1P receptor</p> Signup and view all the answers

    What is the primary consequence of tissue damage induced by leukocyte products activated by T cells?

    <p>Initiation of an immune response</p> Signup and view all the answers

    How are large immune complexes typically processed in the body?

    <p>They are easily removed through phagocytosis</p> Signup and view all the answers

    What process do effector T-lymphocytes undergo at the site of the antigen challenge in delayed-type hypersensitivity?

    <p>They home to the site and secrete cytokines</p> Signup and view all the answers

    What initiates the inflammatory response in Type III hypersensitivity?

    <p>Immune complexes causing tissue injury</p> Signup and view all the answers

    Which of the following best describes the function of MHC II molecules in activated macrophages?

    <p>They are involved in antigen presentation</p> Signup and view all the answers

    What is a likely consequence of the complement activation in Type III hypersensitivity?

    <p>Tissue inflammation and damage</p> Signup and view all the answers

    What type of tests are the skin prick and skin scratch tests classified as?

    <p>Immediate reaction tests</p> Signup and view all the answers

    Which skin test is considered the safest and easiest to perform?

    <p>Skin prick test</p> Signup and view all the answers

    What is a primary concern when using the intradermal test?

    <p>Risk of false positive reactions or anaphylaxis</p> Signup and view all the answers

    What precautions should be taken before conducting skin tests?

    <p>Tests should occur after a resolution of symptoms, ideally within 3 weeks to 3 months</p> Signup and view all the answers

    What is the role of a patch test in skin allergy testing?

    <p>It assesses long-term allergic reactions by fixing the allergen for 1-2 days.</p> Signup and view all the answers

    Which condition is closely associated with the production of large amounts of inflammatory cytokines?

    <p>Toxic shock syndrome</p> Signup and view all the answers

    How long should an allergen be applied in a patch test before reading the results?

    <p>1-2 days with results read after 1 and 2-3 days</p> Signup and view all the answers

    What is a characteristic of superantigen-mediated diseases?

    <p>They lead to systemic reactions akin to septic shock.</p> Signup and view all the answers

    Study Notes

    Hypersensitivity Lecture Notes

    • Hypersensitivity Type II: This reaction involves antibodies (IgG, IgM) reacting with antigens on cell surfaces, or circulating "haptens". Antibodies, including autoantibodies, target foreign or self-antigens. This can lead to cell lysis or dysfunction.

    • Hypersensitivity Type III: Involve immune complexes, comprising antigens and antibodies, forming deposits in blood vessels. This triggers complement activation, inflammation, and tissue damage, which leads to vasculitis.

    • Hypersensitivity Type IV: This delayed hypersensitivity reaction is T-cell mediated. Differentiation into Th1 cells releases IFN-γ, activating macrophages and leading to tissue damage. Takes 24-48 hours to develop.

    Learning Outcomes

    • Antibody-mediated diseases: Understand the mechanisms, clinical syndromes, and therapy for antibody-mediated and immune complex diseases (excluding IgE).
    • Type IV hypersensitivity: Understand the mechanism, clinical syndromes, and therapy for delayed or T cell-mediated Type IV hypersensitivity reactions.
    • Skin Tests: Understand the principles of skin tests used for diagnosing hypersensitivity reactions.

    Hypersensitivity Type II: Tissue Antigens

    • Antibodies targeting tissue antigens deposit on the tissues.
    • IgG binds to Fc receptors on neutrophils and macrophages, activating them.
    • Complement system activation occurs.
    • Inflammation is induced by the release of reactive oxygen species (ROS) and lysosomal enzymes, causing tissue damage.

    Hypersensitivity Type II: Blood Cells

    • Antibodies specific for blood cells bind to them.
    • Opsonization of blood cells occurs.

    Antibody-Mediated Diseases Examples

    • Autoimmune hemolytic anemia: Erythrocyte membrane proteins (Rh blood group antigens and I antigen) affected, resulting in hemolysis and anemia.
    • Idiopathic thrombocytopenic purpura (ITP): Platelet membrane proteins (glycoprotein IIb/IIIa integrin) affected, leading to bleeding.

    Hypersensitivity Type III: Immune Complex-Mediated Reactions

    • Antibodies specific to soluble antigens bind to them.
    • Immune complexes deposit in blood vessels (due to plasma filtration pressure).
    • Complement activation, inflammation, and vasculitis result.

    Different Types of Immune Complex-Mediated Diseases

    • Systemic lupus erythematosus: Targets DNA, nucleoproteins, and other antigens, leading to nephritis, arthritis and vasculitis.
    • Polyarteritis nodosa: The precise antigen is sometimes unclear, but often involves microbial antigens, resulting in vasculitis.
    • Poststreptococcal glomerulonephritis: Streptococcal cell wall antigens form immune complexes, resulting in nephritis.
    • Serum sickness: (clinical and experimental) Various protein antigens lead to systemic vasculitis, nephritis, and arthritis in response to the proteins.
    • Arthus reaction: (experimental) Various protein antigens result in cutaneous vasculitis.

    Immune Complex-Mediated Diseases: Examples

    • Arthus reaction: Localized immune complex deposition due to repeated antigen exposure.
    • Serum sickness: Systemic reaction after exposure to foreign serum.
    • Post-streptococcal glomerulonephritis (PSGN): Immune complexes form in response to a streptococcal infection, leading to kidney damage.
    • Systemic lupus erythematosus (SLE): Autoreactive antibodies target various components of the body, manifesting in multiple organ systems.

    Type IV Hypersensitivity: T-cell Mediated Reactions

    • Th1 cells: Differentiate into Th1 cells, which release IFN-γ, activating macrophages to enhanced phagocytosis, increased enzyme/ROS production, and tissue damage.
    • Macrophages: Activated by Th1 cells, they exhibit increased phagocytic capacity and cytolytic activity.
    • Cytokine Mediated Inflammation: CD4+ T cells are involved. Release of cytokines recruits and activates lymphocytes. This leads to tissue damage, driven by hydrolytic enzymes, O2 intermediates, nitric oxide, and pro-inflammatory cytokines.

    T-Cell Mediated Diseases

    • Type 1 diabetes: Pancreatic islet antigens cause inflammation.
    • Multiple sclerosis (MS): Myelin proteins lead to demyelination.
    • Rheumatoid arthritis: Unknown antigens trigger inflammation in the joint synovium.
    • Contact dermatitis: Chemical substances or drugs acting as haptens triggering inflammatory response.
    • Granulomatous lesions: Infections (TB, Leprosy) that resist macrophage destruction.
    • Superantigen-mediated diseases (toxic shock syndrome): Production of large amounts of pro-inflammatory cytokines causing similar symptoms to septic shock

    Skin Allergy Tests

    • Skin prick: Needle/pin with allergen, immediate reaction.
    • Skin scrape: Remove superficial skin layer and apply.
    • Intradermal: Allergen injected under the skin.
    • Patch test: Patch containing allergen applied to skin.
    • Photopatch test: Patch removed, skin exposed to UV light (for photo-allergic reactions).

    Precautions for Skin Tests

    • Time interval after reaction (3 weeks max).
    • Non-irritant concentrations.
    • Medication history to avoid interference.
    • Physical examination and history for high-risk patients (infection, pregnancy, non-compliance)

    Skin Test Procedures

    • Prick test followed by intradermal test and then patch test.
    • Timing of readings for different tests.
    • Postive and negative controls are necessary to confirm the skin test results.

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    Description

    Test your knowledge on Type II hypersensitivity reactions, including the role of antibodies, complement activation, and the mechanisms involved in tissue damage. This quiz covers various aspects, such as the types of antibodies and how they affect red blood cells. Challenge yourself and enhance your understanding of this critical immunological concept.

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