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Questions and Answers
What type of hypersensitivity is mediated by IgE?
What type of hypersensitivity is mediated by IgE?
Which of the following is NOT considered an atopic condition?
Which of the following is NOT considered an atopic condition?
How do IgE antibodies contribute to hypersensitivity reactions?
How do IgE antibodies contribute to hypersensitivity reactions?
What year did Gell & Coombs define the types of hypersensitivity reactions?
What year did Gell & Coombs define the types of hypersensitivity reactions?
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Which type of hypersensitivity reaction is mediated by T cells?
Which type of hypersensitivity reaction is mediated by T cells?
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What is the first step in the process of sensitization to an allergen?
What is the first step in the process of sensitization to an allergen?
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Which of the following mediators is released by mast cells during allergic reactions?
Which of the following mediators is released by mast cells during allergic reactions?
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What characterizes the late phase of an allergic reaction?
What characterizes the late phase of an allergic reaction?
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Which mediator is primarily responsible for bronchoconstriction during an allergic response?
Which mediator is primarily responsible for bronchoconstriction during an allergic response?
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What is the primary cause of allergy symptoms?
What is the primary cause of allergy symptoms?
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What characterizes Type V hypersensitivity?
What characterizes Type V hypersensitivity?
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Which condition is associated with excess production of thyroid hormones?
Which condition is associated with excess production of thyroid hormones?
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What is a common symptom of Grave's disease?
What is a common symptom of Grave's disease?
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In Type III hypersensitivity, what primarily causes the immune complexes to form?
In Type III hypersensitivity, what primarily causes the immune complexes to form?
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What happens if immune complexes are not cleared effectively?
What happens if immune complexes are not cleared effectively?
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What is the primary role of T helper cells when activated by allergen-presenting cells?
What is the primary role of T helper cells when activated by allergen-presenting cells?
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What triggers anaphylaxis in susceptible individuals?
What triggers anaphylaxis in susceptible individuals?
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Which statement correctly describes Type II hypersensitivity reactions?
Which statement correctly describes Type II hypersensitivity reactions?
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What complication arises from the binding of autoantibodies in Goodpasture’s syndrome?
What complication arises from the binding of autoantibodies in Goodpasture’s syndrome?
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Which of the following conditions is associated with the systemic release of vasoactive mediators?
Which of the following conditions is associated with the systemic release of vasoactive mediators?
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Which type of hypersensitivity is primarily mediated by T cells?
Which type of hypersensitivity is primarily mediated by T cells?
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Which condition is characterized by a collection of macrophages filled with intracellular antigens?
Which condition is characterized by a collection of macrophages filled with intracellular antigens?
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What is the primary immunological trigger for contact hypersensitivity?
What is the primary immunological trigger for contact hypersensitivity?
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In which disease is demyelination primarily targeted at multiple sites in the central nervous system?
In which disease is demyelination primarily targeted at multiple sites in the central nervous system?
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Which hypersensitivity type involves the binding of antibodies to cell receptors, leading to autoimmune conditions?
Which hypersensitivity type involves the binding of antibodies to cell receptors, leading to autoimmune conditions?
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Which condition is known for having prominent granulomas and affects multiple organs, especially the lungs?
Which condition is known for having prominent granulomas and affects multiple organs, especially the lungs?
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What triggers the symptoms in poison ivy contact dermatitis?
What triggers the symptoms in poison ivy contact dermatitis?
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Which disease is an example of Type III hypersensitivity that involves soluble immune complexes?
Which disease is an example of Type III hypersensitivity that involves soluble immune complexes?
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What type of hypersensitivity reaction primarily involves mast cells and IgE?
What type of hypersensitivity reaction primarily involves mast cells and IgE?
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Which of the following is a common characteristic of Crohn's disease?
Which of the following is a common characteristic of Crohn's disease?
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Study Notes
MD137 Immunology - Lecture 4: Allergy & Autoimmunity
- The lecture covers allergy and autoimmunity, hypersensitivity reactions (types I-V), and disease examples.
- Hypersensitivity is an excessive or inappropriate immune reaction causing tissue damage.
- Gell & Coombs (1963) defined and described harmful immune reactions.
- Types I, II, III, and V are antibody-mediated, while Type IV is T cell-mediated.
- Type I Hypersensitivity (IgE-mediated allergy): Immediate hypersensitivity, IgE is produced by B cells, Atopy is a tendency to produce IgE in response to allergens. IgE binds to mast cells, triggering degranulation and release of allergic mediators (e.g., histamine).
- Atopic conditions include eczema, allergic rhinitis, asthma, and food allergies. An allergic trigger might not always be identifiable.
- Sensitization is required for Type I hypersensitivity: First exposure to allergen causes IgE binding to FcεRI receptors on mast cells. Second exposure causes cross-linking of IgE, mast cell degranulation, and allergy symptoms.
- Mast cell mediators include pre-formed mediators (released quickly), enzymes (e.g., tryptase, serotonin, histamine), causing vasodilation, increased vascular permeability, and smooth muscle contraction. Other mediators (e.g., cytokines, lipid mediators) are synthesised later.
- Lipid mediators in allergy include products from Phospholipase A2, Arachidonate, 12-HETE, 12-lipoxygenase, 5-lipoxygenase, 5-HPETE, Lipoxin A, and B, Cyclo-oxygenase, Leukotrienes, PGI2, TXA2, PGF2a, PGD2, PGE2.
- Early/immediate phase of allergy can occur within minutes, caused by primary mediators from mast cells, followed by late phase (occurring 4-24 hours later) due to eosinophils, neutrophils, and T cells, and the release of secondary mediators (e.g., cytokines, lipid mediators). This late phase can be responsible for long-term tissue damage (e.g., tissue remodelling in asthma).
- Allergy symptoms depend on the affected tissue. For the gastrointestinal tract, symptoms include increased fluid secretion and increased peristalsis (e.g., diarrhoea, vomiting), while symptoms in airways include blockage leading to wheezing, coughing, and phlegm. Blood vessels experience increased blood flow and permeability.
- Type I hypersensitivity (also called IgE-mediated allergy) is a common immune response in which B cells produce IgE antibodies. These antibodies bind to allergens, leading to activation and degranulation of mast cells.
- Type II Hypersensitivity (IgM/IgG-mediated): Caused by IgG or IgM binding to antigens on cells or tissues. Bound antibodies activate complement or bind to Fc receptors on phagocytes leading to tissue damage. Goodpasture's syndrome is an example (autoantibodies against a type IV collagen component in the basement membrane of lung and glomeruli leading to inflammation, tissue necrosis, and pulmonary haemorrhage, eventually glomerulonephritis).
- Type III hypersensitivity (Immune complex-mediated): Caused by IgG binding to soluble antigens, forming immune complexes. Clearance mechanisms may become defective, leading to immune complex deposition in tissues, activating complement and releasing inflammatory substances (anaphylatoxins). Vasculitis is an example of this.
- Type IV hypersensitivity (T cell-mediated): Delayed-type hypersensitivity. T cells, and T-cell-driven responses, are responsible for contact dermatitis and chronic diseases like multiple sclerosis (demyelination and sclerosis of nerve tissue). Contact hypersensitivity involves small molecules (haptens, like nickel or chromate) combining with larger tissue proteins; these converted self-antigens become highly immunogenic antigens, resulting in sensitization. Examples include contact dermatitis, multiple sclerosis, Type I diabetes mellitus, and rheumatoid arthritis.
- Granulomatous hypersensitivity develops in response to persistent immune stimuli as collections of macrophages accumulate with intracellular antigens. Examples include Crohn's disease and sarcoidosis.
- Multiple sclerosis (MS) is characterized by demyelination followed by sclerosis of nerve tissue, typically at multiple sites. T cells specific for myelin basic protein in the CNS are implicated.
- Grave's disease (Type V) is a common autoimmune disease, occurring in approximately 1-2% of white Europeans and Americans. Antibodies to the thyroid-stimulating hormone (TSH) receptor cause unregulated stimulation of hormone synthesis, leading to excess thyroid hormones. Common symptoms include goitre, weight loss, and exophthalmos.
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Description
This quiz explores key concepts from Lecture 4 of MD137 Immunology, focusing on allergy and autoimmunity. It covers hypersensitivity reactions, types I to V, and their implications in various diseases. Understand the mechanisms of IgE-mediated allergy and the definition of sensitization in allergic responses.
