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. (D)</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. (D)</p> Signup and view all the answers

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

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

What are the antibodies involved in Type II hypersensitivity reactions?

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

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

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

Which of the following correctly describes Type III hypersensitivity?

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

Which type of hypersensitivity reaction typically involves autoantibodies?

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

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

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

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

<p>Antibodies (C)</p> Signup and view all the answers

What primarily guides T cells to the site of infection?

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

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

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

What happens to CCR7 expression when T cells are activated?

<p>It decreases (C)</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 (C), TNF and IL-4 (D)</p> Signup and view all the answers

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

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

What is the primary consequence of autoimmune hemolytic anemia?

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

In Type III hypersensitivity, what triggers the complement activation?

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

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

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

How do activated macrophages improve their phagocytic ability?

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

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

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

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

<p>Formation of immune complexes (D)</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 (A)</p> Signup and view all the answers

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

<p>Vasculitis (B)</p> Signup and view all the answers

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

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

How are large immune complexes typically processed in the body?

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

What initiates the inflammatory response in Type III hypersensitivity?

<p>Immune complexes causing tissue injury (D)</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 (A)</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 (B)</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 (A)</p> Signup and view all the answers

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

<p>Skin prick test (C)</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 (B)</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 (D)</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. (A)</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 (B)</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 (B)</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. (C)</p> Signup and view all the answers

Flashcards

Type II Hypersensitivity

A type of hypersensitivity reaction where antibodies (IgG or IgM) bind to antigens on cell surfaces, leading to cell destruction.

Type III Hypersensitivity

A type of hypersensitivity reaction where immune complexes form, deposit in tissues, activate complement, and cause inflammation.

Autoimmune Diseases

A group of immune responses triggered by antibodies against self-antigens, leading to various autoimmune diseases.

Haptens

Small molecules that can attach to larger molecules and trigger an immune response when they bind to a cell surface.

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Complement

A protein that can activate complement, a series of proteins in the immune system that helps eliminate pathogens.

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C3a

A molecule released by complement that attracts immune cells to the site of inflammation.

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C5a

A molecule released by complement that amplifies inflammation and attracts immune cells.

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Immune Response

The process of identifying and destroying pathogens or cells that are harmful to the body.

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What is Autoimmunity?

A type of immune reaction where antibodies mistakenly target self-antigens on tissues, leading to damage and inflammation.

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What is Frustrated Phagocytosis?

A process in type II hypersensitivity where antibodies bind to tissue antigens, blocking phagocytosis by immune cells.

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What is the Membrane Attack Complex (MAC)?

Complement activation leads to the formation of a complex that can directly damage cell membranes.

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What happens to red blood cells in Type II hypersensitivity?

In type II hypersensitivity, antibodies target antigens on red blood cells, causing their destruction.

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How do neutrophils contribute to tissue damage in type II hypersensitivity?

Neutrophils release harmful substances like reactive oxygen species (ROS) and proteolytic enzymes, leading to tissue damage.

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Immune Complexes

Molecules formed when antibodies bind to soluble antigens, which can deposit in blood vessels and trigger inflammation.

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Immune Complex Deposition

The process by which immune complexes deposit in blood vessels, leading to inflammation and damage.

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Complement Activation (Type III)

The activation of complement, a system of proteins that helps destroy pathogens, by immune complexes.

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Vasculitis

Inflammation of blood vessels caused by immune complex deposition.

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Immune Complex Clearance

The process of immune complexes being removed from the blood circulation.

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Immune Complex Size Variation

Large, small, and intermediate immune complexes are formed when soluble antigens bind to antibodies.

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Importance of Small Immune Complexes

Immune complexes are usually smaller and less easily cleared, leading to greater risk of inflammation and disease.

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Type IV Hypersensitivity (T-cell Mediated)

A type of immune response where T cells directly attack cells containing specific antigens.

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Th1 Cells

A subset of T helper cells that primarily produce interferon gamma (IFN-γ), which activates macrophages.

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Delayed-type hypersensitivity (DTH)

A type of immune response that happens 24-48 hours after a second exposure to an antigen. It's triggered by memory T cells and involves the release of cytokines.

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Macrophage Activation by IFN-γ

Macrophages increase their ability to engulf and destroy pathogens by expressing more toll-like receptors (TLRs) and other innate immune receptors when activated by IFN-γ.

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Macrophage Cytolytic Activity

Activated macrophages release reactive oxygen species (ROS) and lysosomal enzymes, which contribute to their enhanced killing capacity.

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Macrophage Antigen Presentation

Macrophages increase their expression of MHC II, allowing them to present antigens more effectively to other immune cells.

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Delayed Response in Type IV Hypersensitivity

The time it takes for effector T cells to reach the site of antigen exposure and initiate a response.

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Functional Subsets of T Helper Cells

The cytokine profile of each T cell subset (Th1, Th2, Th17) determines its specific function in the immune response.

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Delayed Immune Response

The delay in the immune response is because T cells need time to migrate to the site of infection.

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T cell Migration

T cells are guided to the site of infection by selectins and chemokine receptors.

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T Cell Receptor Changes

When T cells are activated, their receptor expression changes, helping them move towards the infection.

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Chemokine Recruitment

Chemokines, like C3a and C5a, attract T cells to the site of infection.

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T Cell Migration Process

T cells migrate through blood vessels to the tissue by rolling, adhesion, and transmigration.

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Cytokine Role in T cell Recruitment

Cytokines like TNF and IL-4 produced by CD4+ T cells are key players in attracting T cells to the area.

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Tissue Damage in Immune Response

Tissue damage is caused by leukocyte products, like macrophages, activated by T cells.

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Immune Response Characteristics

Infiltration of T cells and monocytes in tissues, edema, and fibrin deposition caused by increased vascular permeability are hallmarks of the immune response.

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Intracellular Pathogens that Resist Phagocytosis

Organisms that resist destruction by macrophages, such as those causing tuberculosis, leprosy, and schistosomiasis, leading to the formation of giant cells and granulomas.

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Superantigen-Mediated Diseases

A type of immune response where certain bacteria or viruses release toxins called superantigens that bind to T cells, activating large numbers of them in a non-specific way. This leads to excessive production of inflammatory cytokines, causing a condition similar to septic shock.

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Skin Prick Test

A common skin test used to detect allergies. A small amount of allergen is pricked into the skin and the reaction is observed.

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Intradermal Test

A skin test used to detect allergies. A small amount of allergen is injected into the upper layer of the skin, and the reaction is observed.

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Patch Test

A skin test where an allergen patch is applied for 1-2 days, and the reaction is observed after 1 or 2-3 days.

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Photopatch Test

A type of patch test used to detect photoallergies, where the skin is exposed to UV light after the patch is removed.

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Skin Test Timing

Skin tests should be performed at least 3 weeks, but not more than 3 months, after the resolution of symptoms.

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Allergen Concentration in Skin Tests

The concentration of the allergens used in skin tests should be non-irritating.

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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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