Hypersensitivity Reactions Quiz

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80 Questions

What is the principal mechanism of CTL-mediated apoptosis?

Directional delivery of cytotoxic proteins

Which preformed cytotoxic protein forms pores in the plasma membrane of the target cell?

Perforin

What is the function of granzymes in CTL-mediated apoptosis?

Activate caspases, resulting in apoptotic cell death

Which type of T lymphocytes are involved in CTL-mediated apoptosis?

CD8+ T lymphocytes

What is a hypersensitivity reaction?

An altered reactivity to a specific antigen resulting in pathological reactions upon exposure of a sensitised host to that specific antigen.

What characterizes all hypersensitivity reactions?

Sensitisation and effector phases.

When does the pathology associated with hypersensitivity occur?

Effector phase

What distinguishes a beneficial immune response from a harmful hypersensitivity reaction?

Beneficial immune response is immunity, harmful response is hypersensitivity.

Which type of hypersensitivity reaction involves the development of antibodies against cell surface antigens, resulting in cell or tissue destruction?

Type II hypersensitivity

What is the acute systemic reaction mediated by IgE, involving mast cell activation and shock-like symptoms?

Type I hypersensitivity

Which species is noted to be the most sensitive in terms of varying primary target tissues and pathologic findings in anaphylaxis?

Guinea pigs

What inhibits the Th2 response, increasing the likelihood of developing type I hypersensitivity reactions in animals with a predominantly Th2 response?

IFNγ

What is the primary mechanism of tissue damage in type III hypersensitivity reactions?

Activation of complement by antigen-antibody complexes

Which cells are primarily involved in type III hypersensitivity reactions?

FCR-bearing neutrophils and macrophages

What is the time frame required for the development of delayed-type hypersensitivity (DTH) in type IV hypersensitivity?

24 to 48 hours

What is a prototypical example of DTH mediated by CD4+ lymphocytes?

Localised tuberculin response

Which type of hypersensitivity reaction is mediated by an IgE response against environmental antigens?

Type I

What type of hypersensitivity reaction occurs when IgG or IgM is directed against altered self-proteins or foreign antigens?

Type II

Which cells are recruited to sites of Type I hypersensitivity reactions and release toxic granule components and lipid mediators?

Eosinophils

Which factors influence the development of Type I hypersensitivity?

Isotype switching to IgE

What characterizes all hypersensitivity reactions?

Sensitisation and effector phases

When does the pathology associated with hypersensitivity occur?

Effector phase

What distinguishes a beneficial immune response from a harmful hypersensitivity reaction?

Target antigen and location

What is the primary mechanism of tissue damage in type III hypersensitivity reactions?

Immune complex deposition

What is the primary function of perforin in CTL-mediated apoptosis?

Forms pores in the plasma membrane of the target cell

Which molecule is responsible for activating caspases, ultimately resulting in apoptotic cell death in CTL-mediated apoptosis?

Granzymes

In CTL-mediated apoptosis, what is the principal mechanism of delivering cytotoxic proteins to the target cell?

The directional delivery of cytotoxic proteins

Which type of T lymphocytes are primarily involved in CTL-mediated apoptosis?

CD8+ T lymphocytes

Which cells are primarily involved in type III hypersensitivity reactions?

Neutrophils and macrophages

What is the time frame required for the development of delayed-type hypersensitivity (DTH) in type IV hypersensitivity?

24 to 48 hours

What characterizes all hypersensitivity reactions?

Exaggerated immune response

What is the primary mechanism of tissue damage in type III hypersensitivity reactions?

Activation of complement

Which type of MHC molecules have been associated with increased susceptibility to atopy in dogs?

Class I

What is the primary target tissue for anaphylaxis in guinea pigs?

Cardiovascular system

Which antibody-mediated mechanism results in type II hypersensitivity by opsonization and phagocytosis?

Opsonization and phagocytosis

In which disease do antibodies target proteins in intercellular junctions of epidermal cells?

Pemphigus diseases

What role do Th2-type CD4+ lymphocytes and cytokines play in regulating cells involved in Type I hypersensitivity reactions?

Promote the production of IgE and activation of mast cells and eosinophils

What is the primary mechanism of tissue damage in Type III hypersensitivity reactions?

Complement activation and inflammatory reactions

What is the function of eosinophils in Type I hypersensitivity reactions?

Release toxic granule components and lipid mediators, contributing to cell damage

Which cells are primarily involved in Type II hypersensitivity reactions?

Macrophages

What characterizes all hypersensitivity reactions?

Inflammatory reaction in the effector phase

What distinguishes a beneficial immune response from a harmful hypersensitivity reaction?

Intensity and target of the immune response

What is the principal mechanism of tissue damage in type III hypersensitivity reactions?

Immune complex deposition and complement activation

When does the pathology associated with hypersensitivity occur?

Effector phase

What is the principal mechanism of CTL-mediated apoptosis?

Directional delivery of cytotoxic proteins

What is the primary function of perforin in CTL-mediated apoptosis?

Induction of target cell lysis

In CTL-mediated apoptosis, what activates caspases, ultimately resulting in apoptotic cell death?

Granzymes

What is the most common association of DTH mediated by cytotoxic T lymphocytes?

Viral infections

Which type of hypersensitivity reaction involves T lymphocytes and specific antigens?

Type IV

What is the primary mechanism of tissue damage in type III hypersensitivity reactions?

Complement activation

What is the time frame required for the development of delayed-type hypersensitivity (DTH) in type IV hypersensitivity?

24 to 48 hours

Which cells are the primary cells involved in type III hypersensitivity reactions?

Neutrophils and macrophages

Which type of MHC molecules have been associated with increased susceptibility to atopy in dogs?

Class I MHC molecules

What is the acute systemic reaction mediated by IgE, involving mast cell activation and shock-like symptoms?

Systemic type I hypersensitivity

What antigens can elicit systemic anaphylactic reactions?

Drugs, vaccines, insect venom, and heterologous sera

What diseases can result from Type II hypersensitivity in veterinary medicine?

Autoimmune hemolytic anemia, neonatal isoerythrolysis, and pemphigus diseases

What is the primary mechanism of tissue damage in Type III hypersensitivity reactions?

Activation of complement and inflammatory reactions

Which cells are primarily involved in Type II hypersensitivity reactions?

Neutrophils

What inhibits the Th2 response, increasing the likelihood of developing Type I hypersensitivity reactions?

IFN-gamma

What characterizes all hypersensitivity reactions?

Inflammatory responses

What characterizes all hypersensitivity reactions?

They are inappropriate or misdirected responses

When does the pathology associated with hypersensitivity occur?

During the effector phase

What distinguishes a beneficial immune response from a harmful hypersensitivity reaction?

The beneficial effect on the host

What is the function of granzymes in CTL-mediated apoptosis?

Inducing cell lysis

What is the primary mechanism of CTL-mediated apoptosis?

Directional delivery of cytotoxic proteins

Which preformed cytotoxic protein forms pores in the plasma membrane of the target cell?

Perforin

What activates caspases, ultimately resulting in apoptotic cell death in CTL-mediated apoptosis?

Granzymes

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?

Apoptosis

Which type of hypersensitivity reaction involves the formation of insoluble antibody-antigen complexes, leading to complement activation and inflammatory reactions?

Type III

What cells are primarily involved in Type II hypersensitivity reactions?

T lymphocytes

What is the acute systemic reaction mediated by IgE, involving mast cell activation and shock-like symptoms?

Anaphylaxis

What factors influence the development of Type I hypersensitivity?

Mast cell and eosinophil production

Which type of MHC molecules have been associated with increased susceptibility to atopy in dogs?

MHC class II molecules

What is the prototypical example of delayed-type hypersensitivity (DTH) mediated by CD4+ lymphocytes?

Tuberculin skin test reaction

What is the primary target tissue for anaphylaxis in guinea pigs?

Cardiovascular system

What diseases can result from Type II hypersensitivity in veterinary medicine?

All of the above

Which cells are the primary cells involved in type III hypersensitivity reactions?

Neutrophils and macrophages

What factors determine the occurrence of type III hypersensitivity reactions?

Antibody response to antigen quantity and phagocytic system activity

What is the time frame required for the development of delayed-type hypersensitivity (DTH) in type IV hypersensitivity?

24 to 48 hours

What is a prototypical example of DTH mediated by CD4+ lymphocytes?

Localised tuberculin response

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

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.

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