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Questions and Answers
What is a hypersensitivity reaction?
What is a hypersensitivity reaction?
- An altered reactivity to a specific antigen resulting in pathological reactions upon exposure to the antigen (correct)
- An appropriate immune response to combat infections
- An exaggerated but beneficial immune response
- An immune response that occurs at appropriate locations in the body
Why are hypersensitivity reactions characterized as 'hyper'?
Why are hypersensitivity reactions characterized as 'hyper'?
- They are always beneficial to the host
- The reactions elicited are better characterised as inappropriate or misdirected responses (correct)
- They occur with the right intensity
- They are always directed against antigens that pose a threat
What is required for the sensitisation phase of hypersensitivity reactions?
What is required for the sensitisation phase of hypersensitivity reactions?
- No exposure to the antigen
- Previous or prolonged exposure to the antigen (correct)
- Exposure to a harmful antigen
- Exposure to any antigen
What is the most common manifestation of the pathology associated with hypersensitivity reactions?
What is the most common manifestation of the pathology associated with hypersensitivity reactions?
What is the principal mechanism of CTL-mediated apoptosis?
What is the principal mechanism of CTL-mediated apoptosis?
Which proteins are contained in the granules of CTL and contribute to apoptosis?
Which proteins are contained in the granules of CTL and contribute to apoptosis?
What is the role of CD8+ T lymphocytes in DTH mediated by CTLs?
What is the role of CD8+ T lymphocytes in DTH mediated by CTLs?
Which type of hypersensitivity reaction is mediated by IgE and involves mast cell activation and shock-like state?
Which type of hypersensitivity reaction is mediated by IgE and involves mast cell activation and shock-like state?
What is the primary type II hypersensitivity pathogenesis disease mentioned in the text?
What is the primary type II hypersensitivity pathogenesis disease mentioned in the text?
Which molecules are associated with increased susceptibility to atopy in dogs?
Which molecules are associated with increased susceptibility to atopy in dogs?
What is the role of IFNγ in hypersensitivity reactions?
What is the role of IFNγ in hypersensitivity reactions?
Which animals are most sensitive to developing anaphylaxis, according to the text?
Which animals are most sensitive to developing anaphylaxis, according to the text?
What antigens may cause systemic anaphylactic reactions?
What antigens may cause systemic anaphylactic reactions?
In which type of hypersensitivity do antibodies destroy cells or tissues?
In which type of hypersensitivity do antibodies destroy cells or tissues?
What is the role of genetic influences in controlling allergen-specific IgE responses in humans?
What is the role of genetic influences in controlling allergen-specific IgE responses in humans?
Which type of MHC molecules are associated with increased susceptibility to atopy in dogs?
Which type of MHC molecules are associated with increased susceptibility to atopy in dogs?
What is the primary outcome of fatal anaphylaxis?
What is the primary outcome of fatal anaphylaxis?
Which type of hypersensitivity reactions occur at specific tissues or organs, such as skin, respiratory tract, and gastrointestinal tract?
Which type of hypersensitivity reactions occur at specific tissues or organs, such as skin, respiratory tract, and gastrointestinal tract?
Which antibodies are most frequently involved in type II hypersensitivity reactions?
Which antibodies are most frequently involved in type II hypersensitivity reactions?
Which type of hypersensitivity reaction is mediated by an IgE response against environmental antigens?
Which type of hypersensitivity reaction is mediated by an IgE response against environmental antigens?
What type of hypersensitivity reaction occurs when IgG or IgM is directed against altered self-proteins or foreign antigens bound to tissues or cells?
What type of hypersensitivity reaction occurs when IgG or IgM is directed against altered self-proteins or foreign antigens bound to tissues or cells?
Which hypersensitivity reaction results from the formation of insoluble antibody-antigen complexes, leading to complement system activation and inflammatory reactions?
Which hypersensitivity reaction results from the formation of insoluble antibody-antigen complexes, leading to complement system activation and inflammatory reactions?
What is the result of sensitized T lymphocytes' activation to a specific antigen in Type IV hypersensitivity?
What is the result of sensitized T lymphocytes' activation to a specific antigen in Type IV hypersensitivity?
Which disorder is a prototype for Type III hypersensitivity?
Which disorder is a prototype for Type III hypersensitivity?
What plays a crucial role in Type I hypersensitivity, being activated through IgE-mediated and non-IgE-mediated mechanisms?
What plays a crucial role in Type I hypersensitivity, being activated through IgE-mediated and non-IgE-mediated mechanisms?
What do mast cells release during Type I hypersensitivity reactions?
What do mast cells release during Type I hypersensitivity reactions?
Which cells are recruited to the sites of Type I hypersensitivity reactions by chemokines and release toxic granule components and lipid mediators?
Which cells are recruited to the sites of Type I hypersensitivity reactions by chemokines and release toxic granule components and lipid mediators?
What are the factors influencing the development of a Type I hypersensitivity reaction?
What are the factors influencing the development of a Type I hypersensitivity reaction?
Which cytokines influence mast cell production, isotype switching to IgE, and eosinophil maturation and activation in Type I hypersensitivity reactions?
Which cytokines influence mast cell production, isotype switching to IgE, and eosinophil maturation and activation in Type I hypersensitivity reactions?
Which type of hypersensitivity reaction is mainly the result of an IgE-mediated immune response against environmental antigens?
Which type of hypersensitivity reaction is mainly the result of an IgE-mediated immune response against environmental antigens?
What is the result of Type II hypersensitivity?
What is the result of Type II hypersensitivity?
Which type of hypersensitivity reaction involves the formation of antigen-antibody complexes that activate complement and cause tissue damage?
Which type of hypersensitivity reaction involves the formation of antigen-antibody complexes that activate complement and cause tissue damage?
Which cells are primarily involved in type III hypersensitivity reactions?
Which cells are primarily involved in type III hypersensitivity reactions?
What is the main mediator of type IV hypersensitivity reactions?
What is the main mediator of type IV hypersensitivity reactions?
Which disease is commonly associated with type III hypersensitivity reactions?
Which disease is commonly associated with type III hypersensitivity reactions?
What is the role of Th1 cells in type IV hypersensitivity reactions?
What is the role of Th1 cells in type IV hypersensitivity reactions?
Which cells are involved in antibody-mediated disruption of intercellular adhesions in skin diseases?
Which cells are involved in antibody-mediated disruption of intercellular adhesions in skin diseases?
What inhibits acetylcholine binding, causing muscle weakness and down-modulating receptors in myasthenia gravis?
What inhibits acetylcholine binding, causing muscle weakness and down-modulating receptors in myasthenia gravis?
What factors determine a type III hypersensitivity reaction?
What factors determine a type III hypersensitivity reaction?
What is the mechanism of type IV hypersensitivity?
What is the mechanism of type IV hypersensitivity?
What causes localised tuberculin response and contact allergy in humans and animals?
What causes localised tuberculin response and contact allergy in humans and animals?
Which cells are involved in the effector stage responses of type IV hypersensitivity reactions?
Which cells are involved in the effector stage responses of type IV hypersensitivity reactions?
What leads to an inappropriate inflammatory response upon re-exposure in contact allergy?
What leads to an inappropriate inflammatory response upon re-exposure in contact allergy?
Flashcards
Hypersensitivity reaction
Hypersensitivity reaction
An altered reactivity to a specific antigen resulting in pathological reactions upon exposure to the antigen.
Why are hypersensitivity reactions 'hyper'?
Why are hypersensitivity reactions 'hyper'?
The reactions elicited are better characterized as inappropriate or misdirected responses.
What is required for sensitization in hypersensitivity?
What is required for sensitization in hypersensitivity?
Previous or prolonged exposure to the antigen.
Most common manifestation of hypersensitivity pathology?
Most common manifestation of hypersensitivity pathology?
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Principal mechanism of CTL-mediated apoptosis?
Principal mechanism of CTL-mediated apoptosis?
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Proteins in CTL granules that induce apoptosis?
Proteins in CTL granules that induce apoptosis?
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Role of CD8+ T lymphocytes in DTH mediated by CTLs?
Role of CD8+ T lymphocytes in DTH mediated by CTLs?
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Hypersensitivity type mediated by IgE with mast cell activation and shock-like state?
Hypersensitivity type mediated by IgE with mast cell activation and shock-like state?
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Primary Type II hypersensitivity pathogenesis disease?
Primary Type II hypersensitivity pathogenesis disease?
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Molecules associated with atopy susceptibility in dogs?
Molecules associated with atopy susceptibility in dogs?
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Role of IFNγ in hypersensitivity reactions?
Role of IFNγ in hypersensitivity reactions?
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Animals most sensitive to anaphylaxis?
Animals most sensitive to anaphylaxis?
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Antigens that may cause systemic anaphylactic reactions?
Antigens that may cause systemic anaphylactic reactions?
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Hypersensitivity where antibodies destroy cells or tissues?
Hypersensitivity where antibodies destroy cells or tissues?
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Role of genetic influences in controlling allergen-specific IgE responses in humans?
Role of genetic influences in controlling allergen-specific IgE responses in humans?
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MHC molecules associated with increased susceptibility to atopy in dogs?
MHC molecules associated with increased susceptibility to atopy in dogs?
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Primary outcome of fatal anaphylaxis?
Primary outcome of fatal anaphylaxis?
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Hypersensitivity reactions occurring at specific tissues or organs?
Hypersensitivity reactions occurring at specific tissues or organs?
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Antibodies most frequently involved in type II hypersensitivity reactions?
Antibodies most frequently involved in type II hypersensitivity reactions?
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Hypersensitivity reaction mediated by an IgE response against environmental antigens?
Hypersensitivity reaction mediated by an IgE response against environmental antigens?
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Hypersensitivity reaction where IgG or IgM target altered self-proteins or foreign antigens?
Hypersensitivity reaction where IgG or IgM target altered self-proteins or foreign antigens?
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Hypersensitivity reaction involving insoluble antibody-antigen complexes causing inflammation?
Hypersensitivity reaction involving insoluble antibody-antigen complexes causing inflammation?
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Result of sensitized T lymphocyte activation in Type IV hypersensitivity?
Result of sensitized T lymphocyte activation in Type IV hypersensitivity?
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Prototype disease for Type III hypersensitivity?
Prototype disease for Type III hypersensitivity?
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Cells activated through IgE-mediated and non-IgE-mediated mechanisms in Type I hypersensitivity?
Cells activated through IgE-mediated and non-IgE-mediated mechanisms in Type I hypersensitivity?
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Substance released by mast cells during Type I hypersensitivity reactions?
Substance released by mast cells during Type I hypersensitivity reactions?
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Cells recruited to Type I hypersensitivity sites releasing toxic components?
Cells recruited to Type I hypersensitivity sites releasing toxic components?
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Factors influencing development of Type I hypersensitivity reactions?
Factors influencing development of Type I hypersensitivity reactions?
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Cytokines involved in mast cell production, IgE switching, and eosinophil activation in Type I hypersensitivity?
Cytokines involved in mast cell production, IgE switching, and eosinophil activation in Type I hypersensitivity?
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Hypersensitivity reaction mainly caused by IgE-mediated responses against environmental antigens?
Hypersensitivity reaction mainly caused by IgE-mediated responses against environmental antigens?
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Result of Type II hypersensitivity?
Result of Type II hypersensitivity?
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Hypersensitivity reaction involving antigen-antibody complexes causing tissue damage?
Hypersensitivity reaction involving antigen-antibody complexes causing tissue damage?
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Cells involved in type III hypersensitivity reactions?
Cells involved in type III hypersensitivity reactions?
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Main mediator of type IV hypersensitivity reactions?
Main mediator of type IV hypersensitivity reactions?
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Disease commonly associated with type III hypersensitivity reactions?
Disease commonly associated with type III hypersensitivity reactions?
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Role of Th1 cells in type IV hypersensitivity reactions?
Role of Th1 cells in type IV hypersensitivity reactions?
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Cells involved in antibody-mediated disruption of intercellular adhesions in skin diseases?
Cells involved in antibody-mediated disruption of intercellular adhesions in skin diseases?
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What inhibits acetylcholine binding, causing muscle weakness in myasthenia gravis?
What inhibits acetylcholine binding, causing muscle weakness in myasthenia gravis?
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Factors determining a type III hypersensitivity reaction?
Factors determining a type III hypersensitivity reaction?
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Mechanism of type IV hypersensitivity?
Mechanism of type IV hypersensitivity?
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What causes localized tuberculin response and contact allergy?
What causes localized tuberculin response and contact allergy?
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Cells involved in effector stage responses of type IV hypersensitivity?
Cells involved in effector stage responses of type IV hypersensitivity?
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What leads to an inappropriate inflammatory response upon re-exposure in contact allergy?
What leads to an inappropriate inflammatory response upon re-exposure in contact allergy?
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Study Notes
Hypersensitivity Reactions and Their Mechanisms
- Desmoglein 1 is an epidermal cadherin involved in antibody-mediated disruption of intercellular adhesions in skin diseases
- Acetylcholine receptor antibody inhibits acetylcholine binding, causing muscle weakness and down-modulating receptors in myasthenia gravis
- Type III hypersensitivity reactions involve the formation of antigen-antibody complexes that activate complement and cause tissue damage
- FCR-bearing neutrophils and macrophages are the primary cells involved in type III reactions
- Factors determining a type III reaction include the relationship of antibody response to antigen quantity and the activity of the phagocytic system
- Diseases associated with type III reactions are commonly linked to single exposure to a large quantity of antigen or continuous exposure to small quantities
- Examples of type III hypersensitivity diseases include systemic lupus erythematosus, hypersensitivity pneumonia, rheumatoid arthritis, and equine infectious anemia
- Type IV hypersensitivity, also known as delayed-type hypersensitivity, is mediated by T lymphocytes and does not depend on antibodies
- DTH mediated by CD4+ T cells causes localised tuberculin response and contact allergy in humans and animals
- The inflammatory reactions stimulated by CD4+ T cells can be divided into sequential stages involving T-cell activation and effector stage responses
- Th1 cells secrete cytokines, mainly IFN-γ, activating macrophages in type IV hypersensitivity reactions
- Contact allergy in humans and animals involves topical sensitization to an allergen and leads to an inappropriate inflammatory response upon re-exposure.
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