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Questions and Answers
What is the principal mechanism of CTL-mediated apoptosis?
What is the principal mechanism of CTL-mediated apoptosis?
- Release of inflammatory cytokines
- Directional delivery of cytotoxic proteins (correct)
- Activation of macrophages
- Induction of oxidative stress
Which preformed cytotoxic protein forms pores in the plasma membrane of the target cell?
Which preformed cytotoxic protein forms pores in the plasma membrane of the target cell?
- Tumor necrosis factor
- Perforin (correct)
- Granzyme
- Interleukin-2
What is the function of granzymes in CTL-mediated apoptosis?
What is the function of granzymes in CTL-mediated apoptosis?
- Stimulate cell proliferation
- Inhibit the release of cytotoxic proteins
- Activate caspases, resulting in apoptotic cell death (correct)
- Induce DNA repair mechanisms
Which type of T lymphocytes are involved in CTL-mediated apoptosis?
Which type of T lymphocytes are involved in CTL-mediated apoptosis?
What is a hypersensitivity reaction?
What is a hypersensitivity reaction?
What characterizes all hypersensitivity reactions?
What characterizes all hypersensitivity reactions?
When does the pathology associated with hypersensitivity occur?
When does the pathology associated with hypersensitivity occur?
What distinguishes a beneficial immune response from a harmful hypersensitivity reaction?
What distinguishes a beneficial immune response from a harmful hypersensitivity reaction?
Which type of hypersensitivity reaction involves the development of antibodies against cell surface antigens, resulting in cell or tissue destruction?
Which type of hypersensitivity reaction involves the development of antibodies against cell surface antigens, resulting in cell or tissue destruction?
What is the acute systemic reaction mediated by IgE, involving mast cell activation and shock-like symptoms?
What is the acute systemic reaction mediated by IgE, involving mast cell activation and shock-like symptoms?
Which species is noted to be the most sensitive in terms of varying primary target tissues and pathologic findings in anaphylaxis?
Which species is noted to be the most sensitive in terms of varying primary target tissues and pathologic findings in anaphylaxis?
What inhibits the Th2 response, increasing the likelihood of developing type I hypersensitivity reactions in animals with a predominantly Th2 response?
What inhibits the Th2 response, increasing the likelihood of developing type I hypersensitivity reactions in animals with a predominantly Th2 response?
What is the primary mechanism of tissue damage in type III hypersensitivity reactions?
What is the primary mechanism of tissue damage in type III hypersensitivity reactions?
Which cells are primarily involved in type III hypersensitivity reactions?
Which cells are primarily involved in type III hypersensitivity reactions?
What is the time frame required for the development of delayed-type hypersensitivity (DTH) in type IV hypersensitivity?
What is the time frame required for the development of delayed-type hypersensitivity (DTH) in type IV hypersensitivity?
What is a prototypical example of DTH mediated by CD4+ lymphocytes?
What is a prototypical example of DTH mediated by CD4+ lymphocytes?
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?
What type of hypersensitivity reaction occurs when IgG or IgM is directed against altered self-proteins or foreign antigens?
Which cells are recruited to sites of Type I hypersensitivity reactions and release toxic granule components and lipid mediators?
Which cells are recruited to sites of Type I hypersensitivity reactions and release toxic granule components and lipid mediators?
Which factors influence the development of Type I hypersensitivity?
Which factors influence the development of Type I hypersensitivity?
What characterizes all hypersensitivity reactions?
What characterizes all hypersensitivity reactions?
When does the pathology associated with hypersensitivity occur?
When does the pathology associated with hypersensitivity occur?
What distinguishes a beneficial immune response from a harmful hypersensitivity reaction?
What distinguishes a beneficial immune response from a harmful hypersensitivity reaction?
What is the primary mechanism of tissue damage in type III hypersensitivity reactions?
What is the primary mechanism of tissue damage in type III hypersensitivity reactions?
What is the primary function of perforin in CTL-mediated apoptosis?
What is the primary function of perforin in CTL-mediated apoptosis?
Which molecule is responsible for activating caspases, ultimately resulting in apoptotic cell death in CTL-mediated apoptosis?
Which molecule is responsible for activating caspases, ultimately resulting in apoptotic cell death in CTL-mediated apoptosis?
In CTL-mediated apoptosis, what is the principal mechanism of delivering cytotoxic proteins to the target cell?
In CTL-mediated apoptosis, what is the principal mechanism of delivering cytotoxic proteins to the target cell?
Which type of T lymphocytes are primarily involved in CTL-mediated apoptosis?
Which type of T lymphocytes are primarily involved in CTL-mediated apoptosis?
Which cells are primarily involved in type III hypersensitivity reactions?
Which cells are primarily involved in type III hypersensitivity reactions?
What is the time frame required for the development of delayed-type hypersensitivity (DTH) in type IV hypersensitivity?
What is the time frame required for the development of delayed-type hypersensitivity (DTH) in type IV hypersensitivity?
What characterizes all hypersensitivity reactions?
What characterizes all hypersensitivity reactions?
What is the primary mechanism of tissue damage in type III hypersensitivity reactions?
What is the primary mechanism of tissue damage in type III hypersensitivity reactions?
Which type of MHC molecules have been associated with increased susceptibility to atopy in dogs?
Which type of MHC molecules have been associated with increased susceptibility to atopy in dogs?
What is the primary target tissue for anaphylaxis in guinea pigs?
What is the primary target tissue for anaphylaxis in guinea pigs?
Which antibody-mediated mechanism results in type II hypersensitivity by opsonization and phagocytosis?
Which antibody-mediated mechanism results in type II hypersensitivity by opsonization and phagocytosis?
In which disease do antibodies target proteins in intercellular junctions of epidermal cells?
In which disease do antibodies target proteins in intercellular junctions of epidermal cells?
What role do Th2-type CD4+ lymphocytes and cytokines play in regulating cells involved in Type I hypersensitivity reactions?
What role do Th2-type CD4+ lymphocytes and cytokines play in regulating cells involved in Type I hypersensitivity reactions?
What is the primary mechanism of tissue damage in Type III hypersensitivity reactions?
What is the primary mechanism of tissue damage in Type III hypersensitivity reactions?
What is the function of eosinophils in Type I hypersensitivity reactions?
What is the function of eosinophils in Type I hypersensitivity reactions?
Which cells are primarily involved in Type II hypersensitivity reactions?
Which cells are primarily involved in Type II hypersensitivity reactions?
What characterizes all hypersensitivity reactions?
What characterizes all hypersensitivity reactions?
What distinguishes a beneficial immune response from a harmful hypersensitivity reaction?
What distinguishes a beneficial immune response from a harmful hypersensitivity reaction?
What is the principal mechanism of tissue damage in type III hypersensitivity reactions?
What is the principal mechanism of tissue damage in type III hypersensitivity reactions?
When does the pathology associated with hypersensitivity occur?
When does the pathology associated with hypersensitivity occur?
What is the principal mechanism of CTL-mediated apoptosis?
What is the principal mechanism of CTL-mediated apoptosis?
What is the primary function of perforin in CTL-mediated apoptosis?
What is the primary function of perforin in CTL-mediated apoptosis?
In CTL-mediated apoptosis, what activates caspases, ultimately resulting in apoptotic cell death?
In CTL-mediated apoptosis, what activates caspases, ultimately resulting in apoptotic cell death?
What is the most common association of DTH mediated by cytotoxic T lymphocytes?
What is the most common association of DTH mediated by cytotoxic T lymphocytes?
Which type of hypersensitivity reaction involves T lymphocytes and specific antigens?
Which type of hypersensitivity reaction involves T lymphocytes and specific antigens?
What is the primary mechanism of tissue damage in type III hypersensitivity reactions?
What is the primary mechanism of tissue damage in type III hypersensitivity reactions?
What is the time frame required for the development of delayed-type hypersensitivity (DTH) in type IV hypersensitivity?
What is the time frame required for the development of delayed-type hypersensitivity (DTH) in type IV hypersensitivity?
Which cells are the primary cells involved in type III hypersensitivity reactions?
Which cells are the primary cells involved in type III hypersensitivity reactions?
Which type of MHC molecules have been associated with increased susceptibility to atopy in dogs?
Which type of MHC molecules have been associated with increased susceptibility to atopy in dogs?
What is the acute systemic reaction mediated by IgE, involving mast cell activation and shock-like symptoms?
What is the acute systemic reaction mediated by IgE, involving mast cell activation and shock-like symptoms?
What antigens can elicit systemic anaphylactic reactions?
What antigens can elicit systemic anaphylactic reactions?
What diseases can result from Type II hypersensitivity in veterinary medicine?
What diseases can result from Type II hypersensitivity in veterinary medicine?
What is the primary mechanism of tissue damage in Type III hypersensitivity reactions?
What is the primary mechanism of tissue damage in Type III hypersensitivity reactions?
Which cells are primarily involved in Type II hypersensitivity reactions?
Which cells are primarily involved in Type II hypersensitivity reactions?
What inhibits the Th2 response, increasing the likelihood of developing Type I hypersensitivity reactions?
What inhibits the Th2 response, increasing the likelihood of developing Type I hypersensitivity reactions?
What characterizes all hypersensitivity reactions?
What characterizes all hypersensitivity reactions?
What characterizes all hypersensitivity reactions?
What characterizes all hypersensitivity reactions?
When does the pathology associated with hypersensitivity occur?
When does the pathology associated with hypersensitivity occur?
What distinguishes a beneficial immune response from a harmful hypersensitivity reaction?
What distinguishes a beneficial immune response from a harmful hypersensitivity reaction?
What is the function of granzymes in CTL-mediated apoptosis?
What is the function of granzymes in CTL-mediated apoptosis?
What is the primary mechanism of CTL-mediated apoptosis?
What is the primary mechanism of CTL-mediated apoptosis?
Which preformed cytotoxic protein forms pores in the plasma membrane of the target cell?
Which preformed cytotoxic protein forms pores in the plasma membrane of the target cell?
What activates caspases, ultimately resulting in apoptotic cell death in CTL-mediated apoptosis?
What activates caspases, ultimately resulting in apoptotic cell death in CTL-mediated apoptosis?
In CTL-mediated apoptosis, what is the interaction of membrane-bound Fas ligand on the CTL with the Fas receptor on the target cell responsible for?
In CTL-mediated apoptosis, what is the interaction of membrane-bound Fas ligand on the CTL with the Fas receptor on the target cell responsible for?
Which type of hypersensitivity reaction involves the formation of insoluble antibody-antigen complexes, leading to complement activation and inflammatory reactions?
Which type of hypersensitivity reaction involves the formation of insoluble antibody-antigen complexes, leading to complement activation and inflammatory reactions?
What cells are primarily involved in Type II hypersensitivity reactions?
What cells are primarily involved in Type II hypersensitivity reactions?
What is the acute systemic reaction mediated by IgE, involving mast cell activation and shock-like symptoms?
What is the acute systemic reaction mediated by IgE, involving mast cell activation and shock-like symptoms?
What factors influence the development of Type I hypersensitivity?
What factors influence the development of Type I hypersensitivity?
Which type of MHC molecules have been associated with increased susceptibility to atopy in dogs?
Which type of MHC molecules have been associated with increased susceptibility to atopy in dogs?
What is the prototypical example of delayed-type hypersensitivity (DTH) mediated by CD4+ lymphocytes?
What is the prototypical example of delayed-type hypersensitivity (DTH) mediated by CD4+ lymphocytes?
What is the primary target tissue for anaphylaxis in guinea pigs?
What is the primary target tissue for anaphylaxis in guinea pigs?
What diseases can result from Type II hypersensitivity in veterinary medicine?
What diseases can result from Type II hypersensitivity in veterinary medicine?
Which cells are the primary cells involved in type III hypersensitivity reactions?
Which cells are the primary cells involved in type III hypersensitivity reactions?
What factors determine the occurrence of type III hypersensitivity reactions?
What factors determine the occurrence of type III hypersensitivity reactions?
What is the time frame required for the development of delayed-type hypersensitivity (DTH) in type IV hypersensitivity?
What is the time frame required for the development of delayed-type hypersensitivity (DTH) in type IV hypersensitivity?
What is a prototypical example of DTH mediated by CD4+ lymphocytes?
What is a prototypical example of DTH mediated by CD4+ lymphocytes?
Study Notes
Hypersensitivity Reactions and Type I Hypersensitivity
- Hypersensitivity reactions are classified into four types: Type I (immediate), Type II (cytotoxic), Type III (immune complex), and Type IV (delayed-type).
- Type I hypersensitivity is mediated by an IgE response against environmental antigens and can lead to acute inflammatory responses, such as anaphylaxis and allergic dermatitis.
- Type II hypersensitivity occurs when IgG or IgM is directed against altered self-proteins or foreign antigens, leading to tissue or cell destruction.
- Type III hypersensitivity is due to the formation of insoluble antibody-antigen complexes, leading to complement activation and inflammatory reactions.
- Type IV hypersensitivity results from the activation of sensitized T lymphocytes to a specific antigen, causing chronic inflammation.
- Examples of prototype disorders for each type of hypersensitivity include anaphylaxis and allergies for Type I, autoimmune hemolytic anemia for Type II, systemic lupus erythematosus for Type III, and contact dermatitis for Type IV.
- Type I reactions are IgE-mediated and occur in a sensitized host, leading to acute inflammatory processes within minutes of exposure.
- Mast cells, found adjacent to blood vessels and nerves, release preformed (histamine, serotonin) and newly synthesized mediators (arachidonic acid metabolites, cytokines) upon activation.
- Eosinophils are recruited to sites of Type I hypersensitivity reactions and release toxic granule components and lipid mediators, contributing to cell damage.
- The genetic makeup of the host and the dose and route of antigen exposure influence the development of a Type I hypersensitivity reaction.
- Th2-type CD4+ lymphocytes and cytokines (IL3, IL4, IL10) play important roles in regulating cells involved in Type I hypersensitivity reactions.
- Factors influencing the development of Type I hypersensitivity include Th2 response, mast cell and eosinophil production, and isotype switching to IgE.
Hypersensitivity Reactions and Type I Hypersensitivity
- Hypersensitivity reactions are classified into four types: Type I (immediate), Type II (cytotoxic), Type III (immune complex), and Type IV (delayed-type).
- Type I hypersensitivity is mediated by an IgE response against environmental antigens and can lead to acute inflammatory responses, such as anaphylaxis and allergic dermatitis.
- Type II hypersensitivity occurs when IgG or IgM is directed against altered self-proteins or foreign antigens, leading to tissue or cell destruction.
- Type III hypersensitivity is due to the formation of insoluble antibody-antigen complexes, leading to complement activation and inflammatory reactions.
- Type IV hypersensitivity results from the activation of sensitized T lymphocytes to a specific antigen, causing chronic inflammation.
- Examples of prototype disorders for each type of hypersensitivity include anaphylaxis and allergies for Type I, autoimmune hemolytic anemia for Type II, systemic lupus erythematosus for Type III, and contact dermatitis for Type IV.
- Type I reactions are IgE-mediated and occur in a sensitized host, leading to acute inflammatory processes within minutes of exposure.
- Mast cells, found adjacent to blood vessels and nerves, release preformed (histamine, serotonin) and newly synthesized mediators (arachidonic acid metabolites, cytokines) upon activation.
- Eosinophils are recruited to sites of Type I hypersensitivity reactions and release toxic granule components and lipid mediators, contributing to cell damage.
- The genetic makeup of the host and the dose and route of antigen exposure influence the development of a Type I hypersensitivity reaction.
- Th2-type CD4+ lymphocytes and cytokines (IL3, IL4, IL10) play important roles in regulating cells involved in Type I hypersensitivity reactions.
- Factors influencing the development of Type I hypersensitivity include Th2 response, mast cell and eosinophil production, and isotype switching to IgE.
Hypersensitivity Reactions and Type I Hypersensitivity
- Hypersensitivity reactions are classified into four types: Type I (immediate), Type II (cytotoxic), Type III (immune complex), and Type IV (delayed-type).
- Type I hypersensitivity is mediated by an IgE response against environmental antigens and can lead to acute inflammatory responses, such as anaphylaxis and allergic dermatitis.
- Type II hypersensitivity occurs when IgG or IgM is directed against altered self-proteins or foreign antigens, leading to tissue or cell destruction.
- Type III hypersensitivity is due to the formation of insoluble antibody-antigen complexes, leading to complement activation and inflammatory reactions.
- Type IV hypersensitivity results from the activation of sensitized T lymphocytes to a specific antigen, causing chronic inflammation.
- Examples of prototype disorders for each type of hypersensitivity include anaphylaxis and allergies for Type I, autoimmune hemolytic anemia for Type II, systemic lupus erythematosus for Type III, and contact dermatitis for Type IV.
- Type I reactions are IgE-mediated and occur in a sensitized host, leading to acute inflammatory processes within minutes of exposure.
- Mast cells, found adjacent to blood vessels and nerves, release preformed (histamine, serotonin) and newly synthesized mediators (arachidonic acid metabolites, cytokines) upon activation.
- Eosinophils are recruited to sites of Type I hypersensitivity reactions and release toxic granule components and lipid mediators, contributing to cell damage.
- The genetic makeup of the host and the dose and route of antigen exposure influence the development of a Type I hypersensitivity reaction.
- Th2-type CD4+ lymphocytes and cytokines (IL3, IL4, IL10) play important roles in regulating cells involved in Type I hypersensitivity reactions.
- Factors influencing the development of Type I hypersensitivity include Th2 response, mast cell and eosinophil production, and isotype switching to IgE.
Hypersensitivity Reactions: Types and Mechanisms
- Type III hypersensitivity involves antigen-antibody complexes activating complement and causing tissue damage
- The reaction is initiated by antigen-antibody complex formation, leading to inflammation and tissue damage
- FCR-bearing neutrophils and macrophages are the primary cells involved in type III reactions
- Factors determining occurrence of type III reaction include antibody response to antigen quantity and phagocytic system activity
- Diseases associated with type III hypersensitivity result from single or continuous exposure to antigens
- Type IV hypersensitivity, also known as delayed-type hypersensitivity, is mediated by T lymphocytes and specific antigens
- The immune response in type IV hypersensitivity is mediated by direct cytotoxicity or release of soluble cytokines
- The response is dependent on sensitized T lymphocytes and requires 24 to 48 hours to develop
- DTH mediated by CD4+ lymphocytes includes stages of T cell activation and effector responses
- The localised tuberculin response is a prototypical example of DTH mediated by CD4+ lymphocytes
- Another example of type IV hypersensitivity is contact allergy, leading to an inappropriate inflammatory response at the site of challenge
- Type IV hypersensitivity is not dependent on antibody and results from an exaggerated interaction between antigen and cell-mediated immune mechanisms
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Test your knowledge of hypersensitivity reactions and Type I hypersensitivity with this quiz. Explore the classification, mechanisms, and prototype disorders associated with different types of hypersensitivity reactions.
