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Questions and Answers
What distinguishes the type III hypersensitivity reaction from type I in terms of antibodies?
What distinguishes the type III hypersensitivity reaction from type I in terms of antibodies?
Type III hypersensitivity involves IgG antibodies, while type I involves IgE antibodies.
What is the typical time frame for reaching the peak of an Arthus reaction?
What is the typical time frame for reaching the peak of an Arthus reaction?
The Arthus reaction typically peaks at 4-8 hours.
What triggers the condition known as extrinsic allergic alveolitis?
What triggers the condition known as extrinsic allergic alveolitis?
Extrinsic allergic alveolitis is triggered by inhaled antigen complexes with specific IgG in the alveoli.
How does type IV hypersensitivity differ in its initiation compared to types I and III?
How does type IV hypersensitivity differ in its initiation compared to types I and III?
What role do cytokines play in the response of type IV hypersensitivity?
What role do cytokines play in the response of type IV hypersensitivity?
What distinguishes hypersensitivity reactions from protective immune reactions?
What distinguishes hypersensitivity reactions from protective immune reactions?
Describe the mediators involved in Type I hypersensitivity reactions.
Describe the mediators involved in Type I hypersensitivity reactions.
What are the mechanisms through which Type II hypersensitivity leads to tissue damage?
What are the mechanisms through which Type II hypersensitivity leads to tissue damage?
What characterizes Type III hypersensitivity reactions?
What characterizes Type III hypersensitivity reactions?
Explain the role of T cells in Type IV hypersensitivity reactions.
Explain the role of T cells in Type IV hypersensitivity reactions.
How do environmental and genetic factors contribute to hypersensitivity?
How do environmental and genetic factors contribute to hypersensitivity?
What therapeutic strategies are used to manage hypersensitivity reactions?
What therapeutic strategies are used to manage hypersensitivity reactions?
Identify and briefly explain the three groups of damage caused by Type IV hypersensitivity.
Identify and briefly explain the three groups of damage caused by Type IV hypersensitivity.
What activates mast cells in allergic responses?
What activates mast cells in allergic responses?
What is eotaxin and its role in allergic asthma?
What is eotaxin and its role in allergic asthma?
How does genetic susceptibility affect the incidence of allergic diseases?
How does genetic susceptibility affect the incidence of allergic diseases?
What is the ‘hygiene hypothesis’ regarding allergic diseases?
What is the ‘hygiene hypothesis’ regarding allergic diseases?
What causes allergic rhinitis, commonly known as hay fever?
What causes allergic rhinitis, commonly known as hay fever?
What are the life-threatening reactions associated with systemic anaphylaxis?
What are the life-threatening reactions associated with systemic anaphylaxis?
What is the role of environmental factors in developing atopic allergic diseases?
What is the role of environmental factors in developing atopic allergic diseases?
In type I hypersensitivity, what mechanisms lead to symptoms like asthma?
In type I hypersensitivity, what mechanisms lead to symptoms like asthma?
What is the reaction time for a contact hypersensitivity reaction?
What is the reaction time for a contact hypersensitivity reaction?
What histological features are characteristic of contact eczema?
What histological features are characteristic of contact eczema?
In a tuberculin hypersensitivity reaction, which cells are primarily involved?
In a tuberculin hypersensitivity reaction, which cells are primarily involved?
What characterizes a granuloma in delayed hypersensitivity?
What characterizes a granuloma in delayed hypersensitivity?
What is the typical timeframe for granuloma formation?
What is the typical timeframe for granuloma formation?
List one example of an antigen that could lead to contact hypersensitivity.
List one example of an antigen that could lead to contact hypersensitivity.
What type of immune response is elicited by intracellular microorganisms like mycobacteria?
What type of immune response is elicited by intracellular microorganisms like mycobacteria?
Describe the role of TH1 cells in delayed hypersensitivity reactions.
Describe the role of TH1 cells in delayed hypersensitivity reactions.
What determines the type of IgE-mediated allergic reaction?
What determines the type of IgE-mediated allergic reaction?
What are the two main mechanisms by which Type II hypersensitivity leads to cell destruction?
What are the two main mechanisms by which Type II hypersensitivity leads to cell destruction?
What is the main consequence of immune mediated hemolytic anemia (IMHA)?
What is the main consequence of immune mediated hemolytic anemia (IMHA)?
Describe how hemolysis occurs in autoimmune hemolytic anemia (AIHA).
Describe how hemolysis occurs in autoimmune hemolytic anemia (AIHA).
What initiates Rh incompatibility in Rhesus disease?
What initiates Rh incompatibility in Rhesus disease?
What type of antibodies are primarily involved in Type II hypersensitivity reactions?
What type of antibodies are primarily involved in Type II hypersensitivity reactions?
Which effector mechanisms are recruited in the destruction of red blood cells in IMHA?
Which effector mechanisms are recruited in the destruction of red blood cells in IMHA?
In IMHA, where does hemolysis most commonly occur in dogs?
In IMHA, where does hemolysis most commonly occur in dogs?
What role do activated T cells play in macrophage activity?
What role do activated T cells play in macrophage activity?
What is the time frame for IgE-mediated hypersensitivity reactions to occur?
What is the time frame for IgE-mediated hypersensitivity reactions to occur?
Describe the mechanism of antibody-mediated cytotoxic hypersensitivity.
Describe the mechanism of antibody-mediated cytotoxic hypersensitivity.
What causes the local and systemic reactions in immune complex-mediated hypersensitivity?
What causes the local and systemic reactions in immune complex-mediated hypersensitivity?
What cytokines do memory TH1 cells release in cell-mediated hypersensitivity?
What cytokines do memory TH1 cells release in cell-mediated hypersensitivity?
What is the significance of granulomas in the immune response?
What is the significance of granulomas in the immune response?
What is the main mediator for mast cell degranulation in immune complex-mediated hypersensitivity?
What is the main mediator for mast cell degranulation in immune complex-mediated hypersensitivity?
List two examples of conditions that fall under IgE-mediated hypersensitivity.
List two examples of conditions that fall under IgE-mediated hypersensitivity.
Flashcards
Hypersensitivity
Hypersensitivity
An exaggerated or inappropriate immune response that damages the host's tissues.
Type I Hypersensitivity
Type I Hypersensitivity
An immediate hypersensitivity reaction mediated by IgE, activating mast cells.
Type II Hypersensitivity
Type II Hypersensitivity
Hypersensitivity reaction mediated by IgG, targeting cell-surface or matrix antigens, using complement and Fc receptors for attack.
Type III Hypersensitivity
Type III Hypersensitivity
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Type IV Hypersensitivity
Type IV Hypersensitivity
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FcεRI receptors
FcεRI receptors
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Mast cell activation
Mast cell activation
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Eosinophils in asthma
Eosinophils in asthma
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Eosinophil response
Eosinophil response
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Atopic allergy
Atopic allergy
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Type I Hypersensitivity
Type I Hypersensitivity
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Allergic rhinitis
Allergic rhinitis
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Systemic anaphylaxis
Systemic anaphylaxis
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Genetic Susceptibility
Genetic Susceptibility
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Environmental factors
Environmental factors
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Type II Hypersensitivity
Type II Hypersensitivity
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Immune Mediated Hemolytic Anemia (IMHA)
Immune Mediated Hemolytic Anemia (IMHA)
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Autoimmune hemolytic anemia (AIHA)
Autoimmune hemolytic anemia (AIHA)
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Rhesus disease
Rhesus disease
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Complement-mediated lysis
Complement-mediated lysis
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Antibody-dependent cell-mediated cytotoxicity (ADCC)
Antibody-dependent cell-mediated cytotoxicity (ADCC)
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Rh incompatibility
Rh incompatibility
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Dose and Route of Allergen
Dose and Route of Allergen
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Arthus Reaction
Arthus Reaction
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Type III Hypersensitivity
Type III Hypersensitivity
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Extrinsic Allergic Alveolitis
Extrinsic Allergic Alveolitis
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Type IV Hypersensitivity
Type IV Hypersensitivity
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APC (Antigen Presenting Cell)
APC (Antigen Presenting Cell)
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TH1 Cell
TH1 Cell
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FcγRIII
FcγRIII
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IgE-mediated Hypersensitivity
IgE-mediated Hypersensitivity
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Antibody-mediated Cytotoxic Hypersensitivity
Antibody-mediated Cytotoxic Hypersensitivity
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Immune Complex-mediated Hypersensitivity
Immune Complex-mediated Hypersensitivity
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Cell-mediated Hypersensitivity
Cell-mediated Hypersensitivity
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Granuloma Formation
Granuloma Formation
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Cytokine Release
Cytokine Release
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Delayed hypersensitivity reaction time
Delayed hypersensitivity reaction time
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Contact hypersensitivity reaction
Contact hypersensitivity reaction
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Tuberculin reaction
Tuberculin reaction
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Granuloma formation
Granuloma formation
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TH1 influence
TH1 influence
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Delayed Hypersensitivity
Delayed Hypersensitivity
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Granulomas causes
Granulomas causes
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Study Notes
Immunopathology - Hypersensitivity
- Hypersensitivity is the consequence of the immune system causing tissue damage.
- Vaccination, transplantation, transfusion, tolerance generation, allergic reactions, immunodeficiency, and autoimmunity are all topics within immunopathology.
Types of Hypersensitivity
- Gell and Coombs classified hypersensitivity reactions into 4 types.
- Types I, II, and III are antibody-mediated.
- Type IV is T cell-mediated.
- Allergens are antigens that commonly cause hypersensitivity or allergic reactions.
Type I Hypersensitivity (Immediate)
- Caused by contact with an antigen to which the host has a pre-existing IgE antibody.
- IgE is present in low levels in serum (with a half-life of 2-3 days).
- Much of the IgE in the body is bound to high-affinity receptors (FcεRI).
- The bound state of IgE has a longer half-life (~3 weeks).
- Mast cells, eosinophils, and basophils have high-density FcεRI receptors (40-250,000 per cell).
- A wide spectrum of antigen specificities are represented.
- Activation is via cross-linking of FcεRI receptors by antigen binding to bound IgE molecules.
- Mast-cell activation and granule release leads to various symptoms, including:
- Increased fluid secretion and peristalsis in the gastrointestinal tract
- Decreased airways diameter and increased mucus secretion in the airways
- Increased blood flow and permeability in blood vessels
Molecules Released by Mast Cells
- Enzymes (e.g., tryptase, chymase, cathepsin G, carboxypeptidase)
- Toxic mediators (e.g., histamine, heparin)
- Cytokines (e.g., IL-4, IL-13)
- Chemokines (e.g., CCL3)
- Lipid mediators (e.g., prostaglandins D2, E2; leukotrienes B4, C4; platelet-activating factor)
Type II Hypersensitivity
- Mediated by IgG, which engages Fc receptors and complement-mediated effector mechanisms.
- Directed against cell-surface or matrix antigens.
Type III Hypersensitivity
- Mediated by IgG directed against soluble antigens.
- Tissue damage results from Fc receptor and complement-mediated effector mechanisms triggered by immune complexes.
Type IV Hypersensitivity
- T cell-mediated.
- Subdivided into three groups:
- Tissue damage due to macrophage activation by TH1 cells
- Damage caused by TH2 cell activation of inflammatory responses with eosinophils predominant
- Damage directly caused by cytotoxic T cells (CTL)
Incidence and Genetic Susceptibility
- Approximately 20-30% of the population exhibits type I hypersensitivity or atopic allergy to common environmental substances.
- Genetic components play a significant role in atopic allergy.
- Individuals with both atopic parents have a greater than 2x increased likelihood of susceptibility than compared to the overall population.
- Individuals with neither atopic parent have less than 1/2 the likelihood of the general population susceptibility to atopic allergy.
- Various genes influence sensitivity: IL-4, IL-4 receptors, high-affinity IgE receptor β-chain, MHC class II genes, T-cell receptor α locus, and others.
Clinical Aspects of Type I Hypersensitivity
- Allergic rhinitis (hay fever)
- Food allergies
- Atopic (allergic) dermatitis
- Asthma
- Systemic anaphylaxis
Rhesus Disease
- Caused by Rh incompatibility between mother and baby.
- Results from a Rh-negative mother with Rh-positive antibodies towards a Rh-positive baby.
- Can occur after mismatched blood transfusions or fetal blood entering the maternal circulation during miscarriage, abortion, placental bleeding, amniocentesis, or external cephalic version.
Goodpasture's Disease
- Also known as Goodpasture Syndrome or anti-glomerular basement membrane (anti-GBM) disease.
- Uncommon condition causing rapid kidney and lung destruction.
- Anti-GBM antibodies bind to the glomerular basement membrane.
- Treatment typically includes immunosuppressive drugs like steroids.
Myasthenia Gravis (MG)
- Relatively rare autoimmune disorder of peripheral nerves.
- Antibodies form against acetylcholine (ACh) nicotinic postsynaptic receptors at the myoneural junction.
- Leads to a progressive reduction in muscle strength.
- Thymic abnormalities are often associated with MG.
Hypersensitivity Prevention
- Prevention is possible by vaccinating a Rh-negative mother with Rh immune globulin during pregnancy with Rh-positive fetus.
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