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What types of antibodies are involved in Type III hypersensitivity reactions?
What types of antibodies are involved in Type III hypersensitivity reactions?
Type III hypersensitivity reactions are characterized by cell-mediated responses.
Type III hypersensitivity reactions are characterized by cell-mediated responses.
False
What is the Arthus reaction?
What is the Arthus reaction?
A local area of tissue necrosis resulting from acute immune complex vasculitis.
Match the following clinical examples with their corresponding type of hypersensitivity reaction:
Match the following clinical examples with their corresponding type of hypersensitivity reaction:
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In Type III hypersensitivity, immune complexes can deposit in the ______ to cause tissue damage.
In Type III hypersensitivity, immune complexes can deposit in the ______ to cause tissue damage.
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What is Serum Sickness?
What is Serum Sickness?
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Type IV hypersensitivity reactions are mediated primarily by antibodies.
Type IV hypersensitivity reactions are mediated primarily by antibodies.
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What is the mechanism of cytotoxic T cell-mediated killing?
What is the mechanism of cytotoxic T cell-mediated killing?
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What are common clinical features of Systemic Lupus Erythematosus?
What are common clinical features of Systemic Lupus Erythematosus?
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What characterizes Type III hypersensitivity reactions?
What characterizes Type III hypersensitivity reactions?
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Which of the following is an example of a local response in Type III hypersensitivity?
Which of the following is an example of a local response in Type III hypersensitivity?
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What type of antibodies are primarily involved in Type III hypersensitivity reactions?
What type of antibodies are primarily involved in Type III hypersensitivity reactions?
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What causes the Arthus reaction?
What causes the Arthus reaction?
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Which of the following is a systemic example of Type III hypersensitivity?
Which of the following is a systemic example of Type III hypersensitivity?
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Which condition is characterized by autoantibodies against nuclear components?
Which condition is characterized by autoantibodies against nuclear components?
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Which statement is true regarding the immune complexes in Type III hypersensitivity?
Which statement is true regarding the immune complexes in Type III hypersensitivity?
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The Arthus reaction primarily results in which of the following?
The Arthus reaction primarily results in which of the following?
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What is the primary consequence of immune complex deposition in the renal glomeruli?
What is the primary consequence of immune complex deposition in the renal glomeruli?
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Which clinical feature is commonly associated with acute post-streptococcal glomerulonephritis?
Which clinical feature is commonly associated with acute post-streptococcal glomerulonephritis?
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What initiates the formation of immune complexes in serum sickness?
What initiates the formation of immune complexes in serum sickness?
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What type of hypersensitivity is characterized by a delayed response typically occurring 48 to 72 hours after antigen exposure?
What type of hypersensitivity is characterized by a delayed response typically occurring 48 to 72 hours after antigen exposure?
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Which of the following is NOT typically a clinical feature of serum sickness?
Which of the following is NOT typically a clinical feature of serum sickness?
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What is a prominent mechanism used by activated macrophages during a delayed-type hypersensitivity reaction?
What is a prominent mechanism used by activated macrophages during a delayed-type hypersensitivity reaction?
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Which component primarily plays a role in type IV hypersensitivity reactions?
Which component primarily plays a role in type IV hypersensitivity reactions?
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What happens during the inflammatory reaction following immune complex deposition?
What happens during the inflammatory reaction following immune complex deposition?
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What type of inflammation is characterized by a localized collection of epithelioid cells and lymphocytes?
What type of inflammation is characterized by a localized collection of epithelioid cells and lymphocytes?
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Which cells are primarily involved in the tuberculin reaction?
Which cells are primarily involved in the tuberculin reaction?
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What is the primary mechanism by which CD8+ T cells exert their cytotoxic effects?
What is the primary mechanism by which CD8+ T cells exert their cytotoxic effects?
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Which hypersensitivity reaction is exemplified by a reaction against organ transplantation?
Which hypersensitivity reaction is exemplified by a reaction against organ transplantation?
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What is a common clinical manifestation of contact dermatitis arising from delayed-type hypersensitivity?
What is a common clinical manifestation of contact dermatitis arising from delayed-type hypersensitivity?
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In which time frame does induration generally peak after tuberculin injection in a sensitized individual?
In which time frame does induration generally peak after tuberculin injection in a sensitized individual?
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What is the major feature of drug reactions that leads to hypersensitivity?
What is the major feature of drug reactions that leads to hypersensitivity?
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Which type of cell is primarily responsible for granulomatous inflammation?
Which type of cell is primarily responsible for granulomatous inflammation?
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Study Notes
Type III Hypersensitivity
- Characterized by the formation of immune complexes either locally in certain tissues or circulating in the blood and depositing in various tissues.
- Antibodies involved are complement-fixing antibodies, namely IgG, IgM, and occasionally IgA.
- Antigens can be exogenous (foreign proteins like diphtheria antitoxin or those produced by infectious microbes) or endogenous (DNA antigens).
Mechanism of Type III Hypersensitivity
- Immune complexes activate complement, leading to the recruitment of neutrophils and other inflammatory cells.
- The complement activation and neutrophils release inflammatory mediators and enzymes that damage tissues.
Examples of Type III Hypersensitivity
- Arthus Reaction: A localized type III hypersensitivity reaction due to the deposition of immune complexes in blood vessels, often following injections of antigens.
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Systemic Type III Hypersensitivity:
- Serum Sickness: A systemic reaction following exposure to foreign serum proteins, leading to immune complex deposition in various organs.
- Acute Post-Streptococcal Glomerulonephritis: Immune complexes formed against streptococcal antigens deposit in the glomeruli, causing inflammation and damage.
- Systemic Lupus Erythematosus (SLE): Autoantibodies against nuclear components form immune complexes, which deposit in various tissues leading to inflammation & tissue damage.
Clinical Features of Systemic Lupus Erythematosus (SLE)
- Includes fever, fatigue, joint pain, rashes, and kidney problems.
Serum Sickness
- Caused by immune complexes formed against foreign serum proteins.
- Clinical features: fever, urticaria, joint pain, lymph node enlargement, and proteinuria.
Type IV Hypersensitivity
- Characterized by a cell-mediated immune response, mainly involving CD4+ and CD8+ T cells.
- Delayed hypersensitivity reactions, taking 48-72 hours to manifest.
Mechanism of Type IV Hypersensitivity
- Antigens are presented to CD4+ T cells, leading to their activation and the release of cytokines.
- Cytokines recruit macrophages and other inflammatory cells, causing tissue damage.
Granuloma Formation
- Prolonged Type IV reactions can lead to the formation of granulomas, composed of epithelioid cells, lymphocytes, and giant cells.
Clinical Examples of Type IV Hypersensitivity
- Tuberculin Reaction: A classic example of delayed-type hypersensitivity induced by purified protein derivative (PPD) from Mycobacterium tuberculosis.
- Contact Dermatitis: Type IV hypersensitivity caused by chemicals that bind to self proteins, leading to T cell activation and inflammation.
- Drug Reactions: Drug molecules can alter self-proteins, leading to their recognition by T cells and causing allergic reactions.
Direct Cell Toxicity Mediated by CD8+ T Cells
- Cytotoxic T lymphocytes (CTLs) directly kill target cells bearing specific antigens.
- Killing mechanisms: Perforin-granzymes system and Fas ligand.
Examples of Type IV Hypersensitivity
- Reactions against mycobacterial infections (tuberculosis, leprosy).
- Organ transplantation reactions (transplant rejection, graft versus host reaction).
- Reactions against virally infected cells.
- Reactions against malignant cells.
Type III Hypersensitivity (Immune Complex Hypersensitivity)
- Characterized by immune complex formation, either locally in tissues or circulating in the blood and deposited in various tissues.
- Antibodies involved are complement-fixing antibodies, primarily IgG, IgM, and occasionally IgA.
- Antigens can be exogenous (foreign proteins like serum proteins or microbial products) or endogenous (e.g., DNA).
Examples of Localized Type III Hypersensitivity
-
Arthus Reaction: A localized area of tissue necrosis, usually in the skin, resulting from acute immune complex vasculitis.
- Occurs when an antigen is injected intradermally into a previously immunized animal.
- Antigen binds to antibodies in the vascular wall, forming large immune complexes.
- These complexes cause fibrinoid necrosis, thrombosis, and ischemic injury.
Examples of Systemic Type III Hypersensitivity
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Serum Sickness: A reaction that occurred frequently with old vaccines and antibody preparations from other species, but is now less common.
- Occurs when individuals receive antibodies from other individuals or species (e.g., horse or rabbit antithymocyte globulin).
- Pathogenesis involves three phases:
- Formation of immune complexes after antibody formation
- Deposition of immune complexes in blood vessels, renal glomeruli, and joints
- Inflammatory reaction and tissue injury
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Acute Post-streptococcal Glomerulonephritis: Develops 1-2 weeks after a strep throat infection.
- Streptococcal antigens enter the bloodstream, triggering antibody production.
- Antigen-antibody complexes deposit in the basement membrane of glomerular capillaries, leading to inflammation, vasculitis, and endothelial damage.
- Clinically presents with hematuria and oliguria.
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Systemic Lupus Erythematosus (SLE): An autoimmune disease resulting from autoantibodies against nuclear components (DNA, histones).
- These components are normally hidden from the immune system but can be released following tissue injury, such as a viral infection.
- Immune complexes deposit in basement membranes of various tissues, activating complement and causing inflammation and tissue damage.
Type IV Hypersensitivity (Delayed-Type Hypersensitivity)
- Characterized by cell-mediated immune response involving T lymphocytes, primarily CD4+ and CD8+ T cells.
- Reaction is delayed, typically occurring 48 to 72 hours after antigen exposure.
- CD4+ T cells are activated by non-degradable agents such as bacteria, fungi, and protozoa.
Mechanism of Type IV Hypersensitivity
- Activated CD4+ T cells release cytokines, recruiting macrophages and other inflammatory cells to the site of antigen exposure.
- Macrophages become activated and release inflammatory mediators.
- In prolonged DTH reactions, epithelioid cells and giant cells form granulomas around persistent microbes or foreign bodies.
Clinical Examples of Type IV Hypersensitivity
-
Tuberculin Reaction (Mantoux Test): A classic example of DTH.
- Intracutaneous injection of tuberculin (purified protein derivative of Mycobacterium tuberculosis) in a previously sensitized individual.
- Redness and induration appear at the injection site within 8-12 hours, peaking in 24-72 hours.
- Microscopically, the site shows perivascular accumulation of CD4+ T cells and macrophages.
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Contact Dermatitis: A vesicular dermatitis triggered by contact with chemical substances.
- The chemical binds to and modifies self-proteins, leading to their recognition as foreign by T cells and elicitation of a DTH reaction.
- Similar mechanism applies to drug reactions, where drugs can modify self-proteins, including MHC molecules.
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Autoimmune Diseases: DTH plays a role in autoimmune diseases like rheumatoid arthritis and multiple sclerosis.
Direct Cell Toxicity Mediated by CD8+ T Cells
- This type of T cell-mediated injury is caused by CD8+ T lymphocytes (cytotoxic T lymphocytes - CTLs).
- CTLs recognize and kill antigen-bearing target cells, such as virus-infected cells and some tumor cells.
Mechanism of Cytotoxic T Cell–Mediated Killing
- CTLs kill target cells using two main mechanisms:
- Perforin-granzymes system: CTLs release perforin, which creates pores in the target cell membrane. Granzymes, cytotoxic enzymes, then enter the cell through these pores and induce apoptosis.
- Through Fas ligand: CTLs express Fas ligand, which binds to Fas on the target cell, initiating the apoptotic pathway.
Examples of Type IV Hypersensitivity Reactions
- Reactions against mycobacterial infections (e.g., tuberculin reaction, granulomatous reaction in tuberculosis and leprosy)
- Reactions against organ transplantation (e.g., transplant rejection)
- Contact dermatitis
- Autoimmune diseases (e.g., rheumatoid arthritis, multiple sclerosis)
- Some drug reactions
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Description
This quiz covers Type III hypersensitivity, focusing on its characteristics, mechanisms, and examples such as the Arthus reaction and serum sickness. Test your understanding of how immune complexes form and their effects on tissues. Gain insight into the role of antibodies and complement activation in this hypersensitivity type.
