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Questions and Answers
What is the mechanism of cell lysis in Anti-GBM disease?
What is the mechanism of cell lysis in Anti-GBM disease?
Which autoimmune disease is driven by a Th2 response and involves hyperthyroidism?
Which autoimmune disease is driven by a Th2 response and involves hyperthyroidism?
What is the primary mechanism of RBC lysis in ABO blood group incompatibility?
What is the primary mechanism of RBC lysis in ABO blood group incompatibility?
Which antibody-mediated reaction involves IgG binding to cell surface antigens and impairing cell functioning?
Which antibody-mediated reaction involves IgG binding to cell surface antigens and impairing cell functioning?
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What are the initial symptoms of Anti-GBM disease?
What are the initial symptoms of Anti-GBM disease?
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In Graves' Disease, which antibody binds to the TSHR and leads to hyperthyroidism?
In Graves' Disease, which antibody binds to the TSHR and leads to hyperthyroidism?
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What is the primary treatment for Anti-GBM disease?
What is the primary treatment for Anti-GBM disease?
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Which type of hypersensitivity reaction therapy involves daily plasma exchanges for a few weeks?
Which type of hypersensitivity reaction therapy involves daily plasma exchanges for a few weeks?
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What characterizes the involvement of mast cells in autoimmune diseases?
What characterizes the involvement of mast cells in autoimmune diseases?
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What role do neutrophils and macrophages play in complement activation and frustrated phagocytosis?
What role do neutrophils and macrophages play in complement activation and frustrated phagocytosis?
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What is the percentage of the human population that generates a hypersensitivity response to an antigen called an allergen?
What is the percentage of the human population that generates a hypersensitivity response to an antigen called an allergen?
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Which of the following is NOT a type of antigen that can trigger hypersensitivity reactions?
Which of the following is NOT a type of antigen that can trigger hypersensitivity reactions?
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Who placed pollen grains in the nose of patients in 1873 to observe rhinitis as part of immediate hypersensitivity experiments?
Who placed pollen grains in the nose of patients in 1873 to observe rhinitis as part of immediate hypersensitivity experiments?
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What type of response occurs when pollen extract is injected intradermally into patients with immediate hypersensitivity?
What type of response occurs when pollen extract is injected intradermally into patients with immediate hypersensitivity?
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Which immunologist purified IgE from the serum of hay fever patients caused by ragweed exposure in 1967?
Which immunologist purified IgE from the serum of hay fever patients caused by ragweed exposure in 1967?
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What is the consequence of mast cells expressing Fcε receptors with increased affinity for IgE in patients with allergies?
What is the consequence of mast cells expressing Fcε receptors with increased affinity for IgE in patients with allergies?
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What type of cytokines are associated with Th2 differentiation in genetic predisposition for Type I hypersensitivity reactions?
What type of cytokines are associated with Th2 differentiation in genetic predisposition for Type I hypersensitivity reactions?
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Which component's influence leads to dendritic cells producing IL-4 and IL-13 for Th2 differentiation in Type I hypersensitivity reactions?
Which component's influence leads to dendritic cells producing IL-4 and IL-13 for Th2 differentiation in Type I hypersensitivity reactions?
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What happens when allergen epitopes bind to MHC class II molecules in Type I hypersensitivity reactions?
What happens when allergen epitopes bind to MHC class II molecules in Type I hypersensitivity reactions?
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In allergic individuals compared to nonallergic individuals, what is a significant difference regarding Fcε receptors on mast cells?
In allergic individuals compared to nonallergic individuals, what is a significant difference regarding Fcε receptors on mast cells?
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Which cell type is responsible for producing allergen-specific IgE in the sensitization step of the immune response?
Which cell type is responsible for producing allergen-specific IgE in the sensitization step of the immune response?
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What is the primary role of histamine released during mast cell degranulation in allergic reactions?
What is the primary role of histamine released during mast cell degranulation in allergic reactions?
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Which molecule binds to high molecular weight kininogen to promote vasodilation, increased vascular permeability, and recruitment of neutrophils during mast cell degranulation?
Which molecule binds to high molecular weight kininogen to promote vasodilation, increased vascular permeability, and recruitment of neutrophils during mast cell degranulation?
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Which pathway is responsible for the synthesis of leukotrienes, which are 1000-fold more potent than histamine in allergic reactions?
Which pathway is responsible for the synthesis of leukotrienes, which are 1000-fold more potent than histamine in allergic reactions?
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Which secondary mediator is known for recruiting monocytes/macrophages and increasing vascular permeability during allergic reactions?
Which secondary mediator is known for recruiting monocytes/macrophages and increasing vascular permeability during allergic reactions?
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What is the primary mechanism of action of epinephrine in treating systemic anaphylaxis?
What is the primary mechanism of action of epinephrine in treating systemic anaphylaxis?
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Which mediator acts much more rapidly than antihistamines in treating anaphylaxis?
Which mediator acts much more rapidly than antihistamines in treating anaphylaxis?
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In Type II hypersensitivity reactions, what is the outcome when antibodies bind to cell surface receptors and block signaling through them?
In Type II hypersensitivity reactions, what is the outcome when antibodies bind to cell surface receptors and block signaling through them?
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"Frustrated phagocytosis", seen in cytotoxic hypersensitivity, occurs when:
"Frustrated phagocytosis", seen in cytotoxic hypersensitivity, occurs when:
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In Type I hypersensitivities, what is the primary role of IL-4 producing Th2 cells during sensitization?
In Type I hypersensitivities, what is the primary role of IL-4 producing Th2 cells during sensitization?
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Study Notes
Anti-GBM Disease
- Cell lysis in Anti-GBM disease is mediated by antibodies binding to collagen in the glomerular basement membrane, leading to complement activation and inflammatory cell recruitment.
- Initial symptoms include hematuria, proteinuria, and rapid progressive renal failure.
- Primary treatment involves corticosteroids and plasmapheresis to remove antibodies from circulation.
Graves' Disease
- Graves' disease, driven by a Th2 immune response, is characterized by hyperthyroidism due to excessive thyroid hormone production.
- In this disease, antibodies against the Thyroid-Stimulating Hormone Receptor (TSHR) stimulate hormone production.
Blood Group Incompatibility
- RBC lysis in ABO blood group incompatibility primarily occurs through complement activation due to IgM antibodies binding to A or B antigens on transfused red blood cells.
Antibody-Mediated Reactions
- Antibody-mediated reactions involving IgG can impair cell function by binding to cell surface antigens and interfering with normal signaling.
Immune Response Mechanisms
- Neutrophils and macrophages participate in frustrated phagocytosis and contribute to complement activation during autoimmune responses.
- In Type I hypersensitivity reactions, allergen binding to MHC class II molecules activates T helper cells, promoting immune responses.
Hypersensitivity and Allergen Response
- Approximately 20% of the human population generates hypersensitivity responses to allergens.
- Not all antigens trigger hypersensitivity reactions; some proteins and haptens can fail to elicit immune responses.
- Pollen grains were placed in the noses of subjects by researcher Thomas P. Smith in 1873 to study immediate hypersensitivity symptoms like rhinitis.
Allergic Reactions
- Intradermal injection of pollen extract stimulates a Th2 response in patients with immediate hypersensitivity.
- The purification of IgE linked to hay fever was achieved by immunologist Frank A. A. Murphy in 1967.
Mast Cells and Cytokines
- Mast cells expressing high-affinity Fcε receptors for IgE contribute to allergy severity by retaining allergen-bound IgE.
- Th2 differentiation involves cytokines such as IL-4 and IL-13, influenced by the presence of specific components enhancing dendritic cell activation.
Mediators in Allergic Responses
- Release of histamine from mast cell degranulation plays a primary role in increasing vascular permeability and causing bronchoconstriction.
- High molecular weight kininogen binds to bradykinin, promoting vasodilation and neutrophil recruitment.
- Leukotrienes, synthesized via the lipoxygenase pathway, exert more potent effects than histamines, particularly in inflammation.
- Secondary mediators like eosinophil chemotactic factor facilitate the recruitment of monocytes and macrophages.
Anaphylaxis Treatment
- In treating systemic anaphylaxis, epinephrine acts by causing vasoconstriction and bronchodilation, counteracting severe allergic reactions.
- Mediators act more rapidly than antihistamines, effectively alleviating acute allergic symptoms.
Hypersensitivity Outcomes
- In Type II hypersensitivity, binding of antibodies to cell surface receptors can block normal signaling, leading to dysfunction or cell death.
- "Frustrated phagocytosis" occurs when immune cells are unable to ingest pathogens, leading to tissue damage and inflammation.
IL-4 Role in Sensitization
- IL-4 produced by Th2 cells during sensitization drives the production of allergen-specific IgE, establishing an allergic response.
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Description
Learn about antigens, genetic predispositions, cytokines, antibody isotypes, and effector mechanisms of type I and II hypersensitivity reactions. Discover diseases associated with these reactions and understand the mechanisms of action of antihistamines, leukotriene modifying agents, and allergy injections.
