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Questions and Answers
What is the primary mechanism by which Type I hypersensitivity reactions are mediated?
What is the primary mechanism by which Type I hypersensitivity reactions are mediated?
- Complement system activation
- Antibodies of the IgG isotype
- Antibodies of the IgE isotype (correct)
- Cell-mediated response
What is the primary difference between central and peripheral tolerance?
What is the primary difference between central and peripheral tolerance?
- Central tolerance is specific to T-cells, while peripheral tolerance is specific to B-cells
- Central tolerance occurs in the thymus, while peripheral tolerance occurs in the spleen
- Central tolerance involves the negative selection of T-cells, while peripheral tolerance involves the regulation of immune responses (correct)
- Central tolerance is a mechanism of autoimmune disease, while peripheral tolerance is a mechanism of immune suppression
What is the underlying mechanism of Type IV hypersensitivity reactions?
What is the underlying mechanism of Type IV hypersensitivity reactions?
- Complement system activation
- Antibody-mediated response
- Cell-mediated response (correct)
- Inflammation-mediated response
What is the result of a breakdown in tolerance?
What is the result of a breakdown in tolerance?
What is the primary function of mucosal immunity?
What is the primary function of mucosal immunity?
What is the classification system used to categorize hypersensitivity reactions?
What is the classification system used to categorize hypersensitivity reactions?
What is the primary role of Fc receptors in immune complex-mediated disease?
What is the primary role of Fc receptors in immune complex-mediated disease?
What is the characteristic feature of immune complexes that determines their deposition site?
What is the characteristic feature of immune complexes that determines their deposition site?
What is the underlying mechanism of serum sickness?
What is the underlying mechanism of serum sickness?
What is the primary site of immune complex deposition in the Arthus reaction?
What is the primary site of immune complex deposition in the Arthus reaction?
What is the primary consequence of complement deficiencies in immune complex-mediated disease?
What is the primary consequence of complement deficiencies in immune complex-mediated disease?
What is the characteristic feature of systemic lupus erythematosus?
What is the characteristic feature of systemic lupus erythematosus?
What is the primary function of CD8+ CTLs in response to modified self-proteins?
What is the primary function of CD8+ CTLs in response to modified self-proteins?
What type of hypersensitivity reaction is characterized by the formation of granulomas?
What type of hypersensitivity reaction is characterized by the formation of granulomas?
What is the primary cytokine involved in the formation of granulomas?
What is the primary cytokine involved in the formation of granulomas?
What is the primary function of Th1 cells in response to modified self-proteins?
What is the primary function of Th1 cells in response to modified self-proteins?
What is the primary mechanism by which pentadecacatechol in poison ivy leaf interacts with cells?
What is the primary mechanism by which pentadecacatechol in poison ivy leaf interacts with cells?
What is the primary function of APCs in response to modified self-proteins?
What is the primary function of APCs in response to modified self-proteins?
What type of immune response is characterized by the production of IgE antibodies?
What type of immune response is characterized by the production of IgE antibodies?
Which cytokines are produced by Th2 cells and promote the release of IgE and activation of mast cells?
Which cytokines are produced by Th2 cells and promote the release of IgE and activation of mast cells?
What is the mechanism by which IgG antibodies trigger the destruction of cells or tissues in Type II hypersensitivity?
What is the mechanism by which IgG antibodies trigger the destruction of cells or tissues in Type II hypersensitivity?
Which autoimmune disease is caused by autoantibodies targeting the thymic stimulating hormone receptor?
Which autoimmune disease is caused by autoantibodies targeting the thymic stimulating hormone receptor?
What is the primary mechanism of action of autoantibodies in autoimmune haemolytic anaemia?
What is the primary mechanism of action of autoantibodies in autoimmune haemolytic anaemia?
Which type of hypersensitivity is characterized by the participation of eosinophils?
Which type of hypersensitivity is characterized by the participation of eosinophils?
What is the primary function of Th2 cells in allergic reactions?
What is the primary function of Th2 cells in allergic reactions?
Which of the following is NOT a characteristic of Type II hypersensitivity?
Which of the following is NOT a characteristic of Type II hypersensitivity?
What is the mechanism of action of autoantibodies in Goodpasture's syndrome?
What is the mechanism of action of autoantibodies in Goodpasture's syndrome?
Which autoimmune disease is characterized by the presence of autoantibodies against nicotinic acetylcholine receptors?
Which autoimmune disease is characterized by the presence of autoantibodies against nicotinic acetylcholine receptors?
Which organs are typically affected by the accumulation of DNA, histones, RNA binding proteins, and immune complexes in SLE?
Which organs are typically affected by the accumulation of DNA, histones, RNA binding proteins, and immune complexes in SLE?
What is the primary mechanism underlying the development of glomerulonephritis in SLE?
What is the primary mechanism underlying the development of glomerulonephritis in SLE?
What type of hypersensitivity reaction is characterized by the activation of TH1 helper cells, macrophages, and the release of inflammatory cytokines?
What type of hypersensitivity reaction is characterized by the activation of TH1 helper cells, macrophages, and the release of inflammatory cytokines?
What is the primary function of activated macrophages in Type IV hypersensitivity reactions?
What is the primary function of activated macrophages in Type IV hypersensitivity reactions?
What is the term used to describe small molecules that can only elicit an immune response when bound to a larger carrier molecule?
What is the term used to describe small molecules that can only elicit an immune response when bound to a larger carrier molecule?
What is the characteristic time frame for the development of a Type IV hypersensitivity reaction?
What is the characteristic time frame for the development of a Type IV hypersensitivity reaction?
In SLE, immune complex deposition occurs at the glomerular endothelium in kidneys.
In SLE, immune complex deposition occurs at the glomerular endothelium in kidneys.
T cell-mediated immune response is characterized by the production of IgE antibodies.
T cell-mediated immune response is characterized by the production of IgE antibodies.
Haptens can elicit an immune response without binding to a carrier molecule.
Haptens can elicit an immune response without binding to a carrier molecule.
Type IV hypersensitivity reactions involve the activation of eosinophils and mast cells.
Type IV hypersensitivity reactions involve the activation of eosinophils and mast cells.
Autoantibodies in SLE are primarily directed against histones and RNA binding proteins.
Autoantibodies in SLE are primarily directed against histones and RNA binding proteins.
Activated macrophages in Type IV hypersensitivity reactions are less effective at antigen presentation.
Activated macrophages in Type IV hypersensitivity reactions are less effective at antigen presentation.
Type I hypersensitivity reactions are mediated by IgG antibodies.
Type I hypersensitivity reactions are mediated by IgG antibodies.
Th1 cells promote the release of IgE and activation of mast cells in allergic reactions.
Th1 cells promote the release of IgE and activation of mast cells in allergic reactions.
Autoantibodies in autoimmune haemolytic anaemia target the basement membrane collagenase IV.
Autoantibodies in autoimmune haemolytic anaemia target the basement membrane collagenase IV.
Eosinophils are recruited to the lung in asthma through the action of IL-5 and eotaxin.
Eosinophils are recruited to the lung in asthma through the action of IL-5 and eotaxin.
Graves' disease is characterized by autoantibodies targeting the nicotinic acetylcholine receptor.
Graves' disease is characterized by autoantibodies targeting the nicotinic acetylcholine receptor.
Type II hypersensitivity reactions involve the activation of mast cells and the release of histamine.
Type II hypersensitivity reactions involve the activation of mast cells and the release of histamine.
Myasthenia gravis is characterized by autoantibodies targeting the basement membrane collagenase IV.
Myasthenia gravis is characterized by autoantibodies targeting the basement membrane collagenase IV.
Goodpasture's syndrome is an autoimmune disease characterized by autoantibodies targeting the thyroid-stimulating hormone receptor.
Goodpasture's syndrome is an autoimmune disease characterized by autoantibodies targeting the thyroid-stimulating hormone receptor.
Type IV hypersensitivity reactions involve the activation of eosinophils and the release of histamine.
Type IV hypersensitivity reactions involve the activation of eosinophils and the release of histamine.
Asthma is a type of Type II hypersensitivity reaction.
Asthma is a type of Type II hypersensitivity reaction.
Gold is a common allergen that triggers a Type IV hypersensitivity reaction.
Gold is a common allergen that triggers a Type IV hypersensitivity reaction.
Pentadecacatechol in poison ivy leaf can modify extracellular proteins and are presented on MHC class II to CD4+ Th1 cells.
Pentadecacatechol in poison ivy leaf can modify extracellular proteins and are presented on MHC class II to CD4+ Th1 cells.
Th2 cells are involved in the formation of granulomas in Type IV hypersensitivity reactions.
Th2 cells are involved in the formation of granulomas in Type IV hypersensitivity reactions.
Tolerance is a state of excessive immune response to antigens.
Tolerance is a state of excessive immune response to antigens.
CD8+ CTLs kill antigen-expressing cells in Type IV hypersensitivity reactions.
CD8+ CTLs kill antigen-expressing cells in Type IV hypersensitivity reactions.
TNFα is produced by Th1 cells in Type IV hypersensitivity reactions.
TNFα is produced by Th1 cells in Type IV hypersensitivity reactions.
Type II hypersensitivity reactions involve the activation of TH1 helper cells and macrophages.
Type II hypersensitivity reactions involve the activation of TH1 helper cells and macrophages.
Tolerance is a mechanism that prevents the immune system from responding to harmless substances.
Tolerance is a mechanism that prevents the immune system from responding to harmless substances.
Mucosal immunity is primarily mediated by the activation of B cells and the production of IgG antibodies.
Mucosal immunity is primarily mediated by the activation of B cells and the production of IgG antibodies.
Gell and Coombes classification categorizes hypersensitivity reactions into five types, I to V.
Gell and Coombes classification categorizes hypersensitivity reactions into five types, I to V.
Autoimmune diseases occur when there is a breakdown in peripheral tolerance, but not central tolerance.
Autoimmune diseases occur when there is a breakdown in peripheral tolerance, but not central tolerance.
Type IV hypersensitivity reactions are characterized by the formation of granulomas and the activation of TH2 helper cells.
Type IV hypersensitivity reactions are characterized by the formation of granulomas and the activation of TH2 helper cells.
Type III hypersensitivity reactions are characterized by the activation of Th2 cells and the production of IgE antibodies.
Type III hypersensitivity reactions are characterized by the activation of Th2 cells and the production of IgE antibodies.
Complement deficiencies are associated with the formation of soluble immune complexes.
Complement deficiencies are associated with the formation of soluble immune complexes.
The Arthus reaction is a systemic hypersensitivity reaction that occurs in response to injection of poorly catabolised foreign antigens.
The Arthus reaction is a systemic hypersensitivity reaction that occurs in response to injection of poorly catabolised foreign antigens.
Systemic lupus erythematosus is characterized by the presence of autoantibodies against cytoplasmic antigens and DNA.
Systemic lupus erythematosus is characterized by the presence of autoantibodies against cytoplasmic antigens and DNA.
Neutrophil degranulation and vasculitis are characteristic features of Type I hypersensitivity reactions.
Neutrophil degranulation and vasculitis are characteristic features of Type I hypersensitivity reactions.
Th1 cells are involved in the production of IgG antibodies in response to soluble antigens.
Th1 cells are involved in the production of IgG antibodies in response to soluble antigens.
Study Notes
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Type I hypersensitivity reactions are mediated by IgE antibodies and involve mast cells, causing allergic responses to environmental antigens, with symptoms dependent on tissue location.
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In Type I reactions, dendritic cells present antigens to Th2 cells, which produce IL-4, IL-5, and IL-13, leading to IgE production and mast cell activation, resulting in the release of histamine, prostaglandins, and leukotrienes.
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Examples of Type I hypersensitivity reactions include allergic rhinitis and asthma, with treatments targeting IgE production and mast cell activation.
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Type II hypersensitivity reactions are mediated by IgG or IgM antibodies and involve the activation of B cells by Th1 cells, leading to the production of antibodies that target extracellular matrix proteins and connective tissues.
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Type II reactions can be triggered by innocuous foreign antigens, such as those on transfused red blood cells or platelets, or even drugs, and can result in antibody-dependent cellular cytotoxicity (ADCC) or disruption of normal cell function.
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Examples of Type II hypersensitivity reactions include Goodpasture's syndrome, autoimmune haemolytic anaemia, and Graves' disease, with symptoms dependent on the specific target of the antibody response.
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Type III hypersensitivity reactions involve the formation of immune complexes, which can deposit in various tissues depending on their size, leading to the activation of innate immune cells and the production of inflammatory cytokines.
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Examples of Type III hypersensitivity reactions include serum sickness, the Arthus reaction, and systemic lupus erythematosus (SLE), with symptoms dependent on the site of immune complex deposition.
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Type IV hypersensitivity reactions are mediated by T cells, particularly Th1 cells, and involve the activation of macrophages and the production of inflammatory cytokines, leading to delayed-type hypersensitivity (DTH) reactions.
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Examples of Type IV hypersensitivity reactions include contact dermatitis, granulomatous DTH reactions, and diseases such as diabetes type I and rheumatoid arthritis, with symptoms dependent on the specific antigen and site of reaction.
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Hypersensitivity reactions can result from a breakdown in immune regulation and can lead to various diseases, with treatments targeting the specific mechanisms involved in each type of reaction.
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Test your knowledge on the differences between central and peripheral tolerance, mechanisms of autoimmune disease, and types of hypersensitivity responses. Learn about the specialized features of mucosal immunity and how they relate to various diseases.
