MCQs on Immediate and Delayed Hypersensitivity
Immediate and delayed hypersensitivity reactions are two distinct immune responses that occur in response to specific triggers, such as allergens or antigens. Immediate hypersensitivity, also known as Type I hypersensitivity, results in an immediate and rapid reaction upon exposure to the trigger. This type of hypersensitivity involves the release of histamine and other mediators, leading to symptoms like itching, swelling, and wheezing. It is crucial to identify and avoid allergens that trigger immediate hypersensitivity reactions to manage symptoms effectively.
Delayed hypersensitivity, on the other hand, is characterized by a delayed onset, typically occurring within 24 to 72 hours after exposure. This type of hypersensitivity involves the activation of T cells and the release of cytokines, leading to inflammation and tissue damage. Delayed hypersensitivity reactions are commonly seen in conditions like contact dermatitis and certain autoimmune disorders.
Which of the following hypersensitivity occurs via IgE antibody?
a) Type I hypersensitivity
b) Type II hypersensitivity
c) Type III hypersensitivity
d) Type IV hypersensitivity
2) The T helper 1 cell releases cytokines to activate macrophage or T cells and cause direct cellular damage.
Which of the following hypersensitivity reactions are mediated by sensitized T helper-1 cells?
a) Type I hypersensitivity
b) Type II hypersensitivity
c) Type III hypersensitivity
d) Type IV hypersensitivity
3) Which of the following hypersensitivity reactions is a result of massive deposition of immune complex in various tissues, and can induce complement activation and inflammation responses?
a) Type I hypersensitivity
b) Type II hypersensitivity
c) Type III hypersensitivity
d) Type IV hypersensitivity
4) Which of the following hypersensitivity reactions involve antibody-directed complement activation and antibody-dependent cell cytotoxicity?
a) Type I hypersensitivity
b) Type II hypersensitivity
c) Type III hypersensitivity
d) Type IV hypersensitivity
5) When allergen crosslinks with IgE bound to the Fc receptor on the mast cells, the allergen induces the release of mediators.
Which of the following receptor have a high affinity towards IgE?
a) FcεRI
b) FcεRII
c) Both of the above
d) None of the above
6) A hereditary predisposition of the development of immediate hypersensitivity reaction against common environmental antigens are called.........................
a) Atrophy
b) Atopy
c) Anergy
d) Synergy
7) Which of the following domain present in the Fc region of IgE molecule enables the binding of glycoprotein receptors on the surface of the basophils and mast cells?
a)CH1
b)CH2
c) CH3
d) CH4
8) The high-affinity FcεRI receptor functions in signal transduction, activation, and degranulation of chemical mediators such as histamine, leukotrienes, and prostaglandins for the mast cells.
Which of the following intracellular messenger serves this function?
a) Ca++
b) cAMP
c) cGMP
d) None of the above
9) The persistent level of which of the following second messenger inhibits the degranulation of the mast cells and release of the mediators of anaphylaxis?
a) Ca++
b) cAMP
c) cGMP
d) None of the above
10) Which of the following is not an example of Type I hypersensitivity reaction?
a) Asthma
b) Allergic Rhinitis
c) Systemic Lupus Erythematosus
d) Atopic Dermatitis
11) The type I early response occurs within minutes of allergic response.
Which of the following is the early mediator of type I hypersensitivity reaction?
a) Histamine
b) Leukotrienes
c) Prostaglandins
d) All of the above
12) The type I late response occurs hours later and involves the following mediators.
a) IL4
b) IL-5
c) TNF-α
d) All of the above
13) All of the following drugs are involved in increased production or maintenance of cAMP level to prevent anaphylaxis, EXCEPT:
a) Theophylline
b) Epinephrine
c) Cromolyn sodium
d) Cortisone
14) During a blood transfusion, ABO incompatibilities lead to the recognition of A or B antigens present on the RBC resulting in complement-mediated cell lysis.
Which of the following antibody isotype is primarily involved in this type II hypersensitivity reaction?
a) IgG
b) IgM
c) IgE
d) IgA
15) Erythroblastosis fetalis is a severe form of hemolytic disease developed when Rh+ fetus expresses Rh antigen on its blood that the mother does not express.
Which of the following condition is true regarding this condition?
a) During the first pregnancy, the exposure of Rh antigen leads to the generation of memory cells and the IgG response that is harmful during the subsequent pregnancy
b) The condition may be prevented by infusing Rh IgG and reducing exposure to Rh antigen within 24-48 hours of pregnancy
c) Plasmapheresis may be used to remove the antibodies from the circulation
d) All of the above
16) Which of the following drugs can induce all four types of hypersensitive reactions?
a) Penicillin
b) Sulfonamides
c) Local anesthetics
d) Salicylates
17) Which of the following the disease is not the example of type III hypersensitivity reaction?
a) Systemic Lupus Erythematosus
b) Rheumatoid Arthritis
c) Good Pasture’s syndrome
d) Down Syndrome
18) All of the following statement regarding Type III hypersensitivity reaction is true, EXCEPT:
a) Antigen-antibody forms a large complex and is deposited in the nearby tissue
b) Immune complex activate the complement system and anaphylatoxins
b) The anaphylatoxin such as C3a, C3b recruits neutrophils at the site of immune complex deposition
c) Neutrophils and macrophages clear the immune complexes and tissue damage
19) Which of the following statement is not true regarding the sensitization phase of delayed-type hypersensitivity (DTH)?
a) The sensitization phase begins 1-2 weeks after the primary contact with antigens
b) T cell undergo activation and clonal expansion after interacting with antigen-MHC complex
c) CD8+ T Helper-1 cells are primarily activated after exposure to antigen
d) CD4+ T Helper-1 cells are primarily activated after exposure to antigen
20) Which of the following statement is not true regarding the effector phase of delayed-type hypersensitivity (DTH)?
a) The response generally peaks at 48-72 hours after a second exposure to the antigen
b) T Helper 2 cells secrete antibodies and activate antibody-dependent cell cytotoxicity
c) T Helper 2 cells secrete a variety of cytokines that recruit and activate macrophages
d) DTH response becomes self-destructive to the intense response that is visible as the granulomatous reaction.
Bonus Question:
Which of the following cytokines are important for DTH and also used for the diagnosis of Mycobacterium tuberculosis?
a) TNF-α
b) TNF-β
c) IFN-α
d) IFN-γ
Overview of Hypersensitivity
Immune complexes are formed when antigens, such as pathogens or foreign substances, bind to antibodies produced by the immune system. These immune complexes can then accumulate in various tissues and organs, such as the kidneys, skin, and joints, leading to damage and inflammation.
The complement system, a part of the innate immune system, can be activated by these immune complexes and trigger an inflammatory response by attracting immune cells, such as neutrophils and macrophages, to the site of deposition. This can lead to tissue damage and contribute to the development of various autoimmune and inflammatory diseases, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis.
7- d) CH3
10- c) Systemic Lupus ErythematosusAllergic rhinitis: Also known as hay fever, this is a type I hypersensitive reaction to airborne allergens such as pollen, dust mites, and animal dander.
Asthma: Asthma a type I hypersensitivity reaction that can be triggered by allergens, exercise, cold air, or other factors. It causes inflammation and constriction of the airways, leading to wheezing, coughing, and difficulty breathing.
Atopic dermatitis, also known as eczema, is a chronic inflammatory skin condition that is often associated with Type I hypersensitivity reactions. In atopic dermatitis, the immune system reacts to environmental triggers such as pollen, dust mites, and certain foods, leading to inflammation and itching of the skin.
Histamine: Histamine is one of the most well-known and important early mediators. It is stored in mast cells and basophils and is released rapidly in response to an allergen. Histamine can cause a variety of symptoms, including itching, hives, flushing, and bronchoconstriction.
Prostaglandins and leukotrienes: These are lipid mediators that are released from mast cells and other inflammatory cells. They contribute to inflammation, bronchoconstriction, and vascular permeability.
12- d) All of the above
Methylxanthines: Methylxanthines such as theophylline can increase the production of cAMP in a variety of cells, including mast cells and basophils. These drugs are less commonly used for the prevention of anaphylaxis due to their potential side effects and interactions with other drugs.
Cromolyn sodium: Cromolyn sodium is a mast cell stabilizer that inhibits the release of histamine and other mediators from mast cells by increasing the levels of cAMP. It is often used to prevent asthma attacks and can also be used to prevent anaphylaxis in patients with allergies.
Epinephrine: Epinephrine is a hormone that can stimulate the production of cAMP in a variety of cells, including mast cells and basophils. It is the first-line treatment for anaphylaxis and can be administered as an injection in cases of severe allergic reactions.
Type I hypersensitivity reactions are the most common and immediate, and can lead to anaphylaxis. Type II, III, and IV hypersensitivity reactions can be delayed and are less common.
Penicillin can cause a type I hypersensitivity reaction by binding to serum proteins to form a hapten-carrier complex, which can trigger the production of IgE antibodies. It can also cause type II hypersensitivity reactions by binding to cell surface proteins and triggering complement-mediated lysis or antibody-dependent cell-mediated cytotoxicity. Penicillin can cause type III hypersensitivity reactions by forming immune complexes with penicillin and self-antigens that deposit in tissues and trigger complement activation and inflammation. Finally, penicillin can cause type IV hypersensitivity reactions by inducing a delayed T-cell-mediated response.
19- c) CD8+ T Helper-1 cells are primarily activated after exposure to antigen
Delayed hypersensitivity, on the other hand, is characterized by a delayed onset, typically occurring within 24 to 72 hours after exposure. This type of hypersensitivity involves the activation of T cells and the release of cytokines, leading to inflammation and tissue damage. Delayed hypersensitivity reactions are commonly seen in conditions like contact dermatitis and certain autoimmune disorders.
1) Hypersensitivity reactions are broadly classified into four different types.
Which of the following hypersensitivity occurs via IgE antibody?
a) Type I hypersensitivity
b) Type II hypersensitivity
c) Type III hypersensitivity
d) Type IV hypersensitivity
2) The T helper 1 cell releases cytokines to activate macrophage or T cells and cause direct cellular damage.
Which of the following hypersensitivity reactions are mediated by sensitized T helper-1 cells?
a) Type I hypersensitivity
b) Type II hypersensitivity
c) Type III hypersensitivity
d) Type IV hypersensitivity
3) Which of the following hypersensitivity reactions is a result of massive deposition of immune complex in various tissues, and can induce complement activation and inflammation responses?
a) Type I hypersensitivity
b) Type II hypersensitivity
c) Type III hypersensitivity
d) Type IV hypersensitivity
4) Which of the following hypersensitivity reactions involve antibody-directed complement activation and antibody-dependent cell cytotoxicity?
a) Type I hypersensitivity
b) Type II hypersensitivity
c) Type III hypersensitivity
d) Type IV hypersensitivity
5) When allergen crosslinks with IgE bound to the Fc receptor on the mast cells, the allergen induces the release of mediators.
Which of the following receptor have a high affinity towards IgE?
a) FcεRI
b) FcεRII
c) Both of the above
d) None of the above
6) A hereditary predisposition of the development of immediate hypersensitivity reaction against common environmental antigens are called.........................
a) Atrophy
b) Atopy
c) Anergy
d) Synergy
7) Which of the following domain present in the Fc region of IgE molecule enables the binding of glycoprotein receptors on the surface of the basophils and mast cells?
a)CH1
b)CH2
c) CH3
d) CH4
8) The high-affinity FcεRI receptor functions in signal transduction, activation, and degranulation of chemical mediators such as histamine, leukotrienes, and prostaglandins for the mast cells.
Which of the following intracellular messenger serves this function?
a) Ca++
b) cAMP
c) cGMP
d) None of the above
9) The persistent level of which of the following second messenger inhibits the degranulation of the mast cells and release of the mediators of anaphylaxis?
a) Ca++
b) cAMP
c) cGMP
d) None of the above
10) Which of the following is not an example of Type I hypersensitivity reaction?
a) Asthma
b) Allergic Rhinitis
c) Systemic Lupus Erythematosus
d) Atopic Dermatitis
11) The type I early response occurs within minutes of allergic response.
Which of the following is the early mediator of type I hypersensitivity reaction?
a) Histamine
b) Leukotrienes
c) Prostaglandins
d) All of the above
12) The type I late response occurs hours later and involves the following mediators.
a) IL4
b) IL-5
c) TNF-α
d) All of the above
13) All of the following drugs are involved in increased production or maintenance of cAMP level to prevent anaphylaxis, EXCEPT:
a) Theophylline
b) Epinephrine
c) Cromolyn sodium
d) Cortisone
14) During a blood transfusion, ABO incompatibilities lead to the recognition of A or B antigens present on the RBC resulting in complement-mediated cell lysis.
Which of the following antibody isotype is primarily involved in this type II hypersensitivity reaction?
a) IgG
b) IgM
c) IgE
d) IgA
15) Erythroblastosis fetalis is a severe form of hemolytic disease developed when Rh+ fetus expresses Rh antigen on its blood that the mother does not express.
Which of the following condition is true regarding this condition?
a) During the first pregnancy, the exposure of Rh antigen leads to the generation of memory cells and the IgG response that is harmful during the subsequent pregnancy
b) The condition may be prevented by infusing Rh IgG and reducing exposure to Rh antigen within 24-48 hours of pregnancy
c) Plasmapheresis may be used to remove the antibodies from the circulation
d) All of the above
16) Which of the following drugs can induce all four types of hypersensitive reactions?
a) Penicillin
b) Sulfonamides
c) Local anesthetics
d) Salicylates
17) Which of the following the disease is not the example of type III hypersensitivity reaction?
a) Systemic Lupus Erythematosus
b) Rheumatoid Arthritis
c) Good Pasture’s syndrome
d) Down Syndrome
18) All of the following statement regarding Type III hypersensitivity reaction is true, EXCEPT:
a) Antigen-antibody forms a large complex and is deposited in the nearby tissue
b) Immune complex activate the complement system and anaphylatoxins
b) The anaphylatoxin such as C3a, C3b recruits neutrophils at the site of immune complex deposition
c) Neutrophils and macrophages clear the immune complexes and tissue damage
19) Which of the following statement is not true regarding the sensitization phase of delayed-type hypersensitivity (DTH)?
a) The sensitization phase begins 1-2 weeks after the primary contact with antigens
b) T cell undergo activation and clonal expansion after interacting with antigen-MHC complex
c) CD8+ T Helper-1 cells are primarily activated after exposure to antigen
d) CD4+ T Helper-1 cells are primarily activated after exposure to antigen
20) Which of the following statement is not true regarding the effector phase of delayed-type hypersensitivity (DTH)?
a) The response generally peaks at 48-72 hours after a second exposure to the antigen
b) T Helper 2 cells secrete antibodies and activate antibody-dependent cell cytotoxicity
c) T Helper 2 cells secrete a variety of cytokines that recruit and activate macrophages
d) DTH response becomes self-destructive to the intense response that is visible as the granulomatous reaction.
Bonus Question:
Which of the following cytokines are important for DTH and also used for the diagnosis of Mycobacterium tuberculosis?
a) TNF-α
b) TNF-β
c) IFN-α
d) IFN-γ
Overview of Hypersensitivity
- Type I hypersensitivity: This is also known as immediate hypersensitivity, and it is mediated by IgE antibodies. In this type of reaction, the body's immune system produces IgE antibodies in response to an allergen, such as pollen or certain foods. When the person is exposed to the allergen again, the allergen binds to the IgE antibodies on mast cells and basophils, triggering the release of histamine and other inflammatory mediators. This can cause symptoms ranging from mild itching and hives to severe anaphylaxis.
- Type II hypersensitivity: This is also known as cytotoxic hypersensitivity, and it is mediated by IgG or IgM antibodies that recognize and bind to specific antigens on the surface of cells or tissues, leading to their destruction. This type of reaction is involved in autoimmune diseases such as autoimmune hemolytic anemia and some drug-induced immune reactions.
- Type III hypersensitivity: This is also known as immune complex hypersensitivity, and it is mediated by the formation of immune complexes that deposit in various tissues, leading to inflammation and tissue damage. This type of reaction is involved in autoimmune diseases such as systemic lupus erythematosus and certain infections.
- Type IV hypersensitivity: This is also known as delayed-type hypersensitivity, and it is mediated by T cells. In this type of reaction, T cells that are sensitized to a specific antigen recognize and respond to the antigen upon subsequent exposure, leading to an inflammatory reaction. This type of reaction is involved in contact dermatitis, certain infections, and some autoimmune diseases.
Multiple Choice Answers:
1- a) Type I hypersensitivity
Type I hypersensitivity occur via IgE antibody. In Type I hypersensitivity, an individual's immune system overreacts allergen, and produces a large amount of IgE antibodies specific to that allergen. When the individual is exposed to the allergen again, the allergen binds to the IgE antibodies, causing the release of histamine and other inflammatory mediators from mast cells and basophils, leading to an allergic reaction. Examples of Type I hypersensitivity reactions include allergic rhinitis (hay fever), asthma, and anaphylaxis
2- d) Type IV hypersensitivity
1- a) Type I hypersensitivity
Type I hypersensitivity occur via IgE antibody. In Type I hypersensitivity, an individual's immune system overreacts allergen, and produces a large amount of IgE antibodies specific to that allergen. When the individual is exposed to the allergen again, the allergen binds to the IgE antibodies, causing the release of histamine and other inflammatory mediators from mast cells and basophils, leading to an allergic reaction. Examples of Type I hypersensitivity reactions include allergic rhinitis (hay fever), asthma, and anaphylaxis
2- d) Type IV hypersensitivity
Type IV hypersensitivity reactions, which are also known as delayed-type hypersensitivity reactions, are primarily mediated by sensitized Th1 cells. In this type of reaction, antigen-specific Th1 cells are activated upon re-exposure to the antigen, leading to the recruitment of macrophages and other immune cells to the site of inflammation. This type of reaction is involved in contact dermatitis, tuberculin reactions, and certain autoimmune diseases.
3- c) Type III hypersensitivity
Type III hypersensitivity occurs when there is an excessive formation and deposition of immune complexes in various tissues and organs, leading to activation of the complement system and triggering an inflammatory response.Immune complexes are formed when antigens, such as pathogens or foreign substances, bind to antibodies produced by the immune system. These immune complexes can then accumulate in various tissues and organs, such as the kidneys, skin, and joints, leading to damage and inflammation.
The complement system, a part of the innate immune system, can be activated by these immune complexes and trigger an inflammatory response by attracting immune cells, such as neutrophils and macrophages, to the site of deposition. This can lead to tissue damage and contribute to the development of various autoimmune and inflammatory diseases, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis.
4- b) Type II hypersensitivity
Type II hypersensitivity reactions involve the binding of antibodies, typically IgG or IgM, to antigens on the surface of cells or tissues, resulting in activation of the complement system and destruction of the target cells. This process is known as antibody-directed complement activation. Examples of Type II hypersensitivity reactions include autoimmune hemolytic anemia and transfusion reactions.5- a) FcεRI
The receptor that has a high affinity towards IgE antibodies is called the high-affinity IgE receptor, or FcεRI. This receptor is expressed on the surface of certain immune cells, such as mast cells, basophils, and eosinophils, as well as some dendritic cells.
When IgE antibodies bind to their specific antigens, such as allergens, they can also bind to FcεRI on the surface of mast cells and basophils. This binding leads to cross-linking of the FcεRI receptors and activation of the immune cells, which can release inflammatory mediators such as histamine, leukotrienes, and cytokines.
When IgE antibodies bind to their specific antigens, such as allergens, they can also bind to FcεRI on the surface of mast cells and basophils. This binding leads to cross-linking of the FcεRI receptors and activation of the immune cells, which can release inflammatory mediators such as histamine, leukotrienes, and cytokines.
6- b) Atopy
The hereditary predisposition of the development of immediate hypersensitivity reactions against common environmental antigens is called atopy. Individuals with atopy have an increased likelihood of developing allergies, such as allergic rhinitis (hay fever), asthma, and atopic dermatitis (eczema), when exposed to certain environmental triggers, such as pollen, dust mites, or animal dander. Atopy is thought to result from a complex interplay between genetic and environmental factors.7- d) CH3
The CH3 domain present in the Fc region of the IgE molecule enables the binding of glycoprotein receptors on the surface of basophils and mast cells. These receptors, known as FcεRI (Fc epsilon receptor I), bind to the CH3 domain of IgE and trigger a signaling cascade that leads to the release of histamine and other inflammatory mediators from the basophils and mast cells. This process is important in the pathophysiology of allergic reactions, including allergic rhinitis, asthma, and anaphylaxis.
8- a) Ca++
When IgE molecules bind to the FcεRI receptors on the surface of mast cells and basophils, the receptors cluster together and become phosphorylated on their intracellular domains by the enzyme Lyn. This phosphorylation recruits and activates downstream signaling molecules, including Syk and the adapter protein LAT, which then activate various enzymes and transcription factors.
These signaling pathways ultimately lead to the activation of phospholipase C, which cleaves phosphatidylinositol 4,5-bisphosphate (PIP2) into inositol triphosphate (IP3) and diacylglycerol (DAG). IP3 causes the release of calcium ions from intracellular stores, which then trigger the exocytosis of pre-formed granules containing inflammatory mediators, such as histamine. DAG, on the other hand, activates protein kinase C, which can lead to the production of additional inflammatory mediators, such as leukotrienes and cytokines.
These signaling pathways ultimately lead to the activation of phospholipase C, which cleaves phosphatidylinositol 4,5-bisphosphate (PIP2) into inositol triphosphate (IP3) and diacylglycerol (DAG). IP3 causes the release of calcium ions from intracellular stores, which then trigger the exocytosis of pre-formed granules containing inflammatory mediators, such as histamine. DAG, on the other hand, activates protein kinase C, which can lead to the production of additional inflammatory mediators, such as leukotrienes and cytokines.
9- b) cAMP
The persistent level of a second messenger called cyclic AMP (cAMP) can inhibit the degranulation of mast cells and the release of mediators of anaphylaxis such as histamine, leukotrienes, and prostaglandins. This occurs because cAMP activates protein kinase A (PKA), which in turn inhibits the activity of several key enzymes involved in the degranulation process.
10- c) Systemic Lupus Erythematosus
Asthma: Asthma a type I hypersensitivity reaction that can be triggered by allergens, exercise, cold air, or other factors. It causes inflammation and constriction of the airways, leading to wheezing, coughing, and difficulty breathing.
Atopic dermatitis, also known as eczema, is a chronic inflammatory skin condition that is often associated with Type I hypersensitivity reactions. In atopic dermatitis, the immune system reacts to environmental triggers such as pollen, dust mites, and certain foods, leading to inflammation and itching of the skin.
11- d) All of the above
The early mediators of Type I hypersensitivity reactions are released within minutes to hours after exposure to an allergen and include:Histamine: Histamine is one of the most well-known and important early mediators. It is stored in mast cells and basophils and is released rapidly in response to an allergen. Histamine can cause a variety of symptoms, including itching, hives, flushing, and bronchoconstriction.
Prostaglandins and leukotrienes: These are lipid mediators that are released from mast cells and other inflammatory cells. They contribute to inflammation, bronchoconstriction, and vascular permeability.
12- d) All of the above
IL-4 is a cytokine that is released early in the allergic response and plays a key role in the development and maintenance of Th2 cells, which are important for the production of IgE antibodies. IL-4 also contributes to the recruitment and activation of eosinophils and other inflammatory cells.
IL-5 is a cytokine that is released by Th2 cells and is important for the development, activation, and survival of eosinophils. Eosinophils play a key role in the pathogenesis of allergic diseases, including asthma and allergic rhinitis.
TNF-alpha is a pro-inflammatory cytokine that is released by mast cells and other inflammatory cells. It contributes to the recruitment and activation of other immune cells, including eosinophils, neutrophils, and T cells. TNF-alpha also plays a role in the development and maintenance of chronic inflammation in allergic diseases.
IL-5 is a cytokine that is released by Th2 cells and is important for the development, activation, and survival of eosinophils. Eosinophils play a key role in the pathogenesis of allergic diseases, including asthma and allergic rhinitis.
TNF-alpha is a pro-inflammatory cytokine that is released by mast cells and other inflammatory cells. It contributes to the recruitment and activation of other immune cells, including eosinophils, neutrophils, and T cells. TNF-alpha also plays a role in the development and maintenance of chronic inflammation in allergic diseases.
13)- c) Cromolyn sodium
Beta-agonists: Beta-agonists such as albuterol and salmeterol can stimulate the production of cAMP in airway smooth muscle cells and inhibit mast cell degranulation. These drugs are commonly used to treat asthma and can be used to prevent anaphylaxis in patients with known allergies.Methylxanthines: Methylxanthines such as theophylline can increase the production of cAMP in a variety of cells, including mast cells and basophils. These drugs are less commonly used for the prevention of anaphylaxis due to their potential side effects and interactions with other drugs.
Cromolyn sodium: Cromolyn sodium is a mast cell stabilizer that inhibits the release of histamine and other mediators from mast cells by increasing the levels of cAMP. It is often used to prevent asthma attacks and can also be used to prevent anaphylaxis in patients with allergies.
Epinephrine: Epinephrine is a hormone that can stimulate the production of cAMP in a variety of cells, including mast cells and basophils. It is the first-line treatment for anaphylaxis and can be administered as an injection in cases of severe allergic reactions.
14- b) IgM
The antibody isotype that is primarily involved in ABO incompatibility reactions during blood transfusion is IgM. IgM antibodies are naturally occurring antibodies that are produced against A and B antigens early in life, regardless of whether an individual has been exposed to these antigens. When a person receives a blood transfusion with ABO-incompatible blood, the pre-existing IgM antibodies in the recipient's serum bind to the A or B antigens on the transfused red blood cells, leading to complement activation and subsequent hemolysis. In addition to IgM, IgG antibodies may also be produced in response to ABO-incompatible blood transfusion, but IgM is the primary antibody involved in this type II hypersensitivity reaction.
15- d) All of the above
The exposure of Rh antigen leads to the generation of memory cells and the IgG response that is harmful during the subsequent pregnancy.
Erythroblastosis fetalis is a severe form of hemolytic disease that can occur when a Rh-negative mother is pregnant with a Rh-positive fetus. During delivery or any other event causing mixing of the fetal and maternal blood, Rh antigens from the fetal RBCs can enter the maternal circulation, leading to the production of Rh-specific antibodies by the mother's immune system. These antibodies can then cross the placenta and cause hemolysis of fetal RBCs, leading to anemia, jaundice, and other complications.
During the first pregnancy, the mother is exposed to Rh antigens for the first time, leading to the generation of memory B cells and the production of IgG antibodies against Rh antigens. These memory B cells can persist for years and lead to a rapid and robust IgG response in subsequent pregnancies with Rh-positive fetuses, leading to severe hemolytic disease.
Erythroblastosis fetalis is a severe form of hemolytic disease that can occur when a Rh-negative mother is pregnant with a Rh-positive fetus. During delivery or any other event causing mixing of the fetal and maternal blood, Rh antigens from the fetal RBCs can enter the maternal circulation, leading to the production of Rh-specific antibodies by the mother's immune system. These antibodies can then cross the placenta and cause hemolysis of fetal RBCs, leading to anemia, jaundice, and other complications.
During the first pregnancy, the mother is exposed to Rh antigens for the first time, leading to the generation of memory B cells and the production of IgG antibodies against Rh antigens. These memory B cells can persist for years and lead to a rapid and robust IgG response in subsequent pregnancies with Rh-positive fetuses, leading to severe hemolytic disease.
16- a) Penicillin
Penicillin is a drug that can induce all four types of hypersensitivity reactions.Type I hypersensitivity reactions are the most common and immediate, and can lead to anaphylaxis. Type II, III, and IV hypersensitivity reactions can be delayed and are less common.
Penicillin can cause a type I hypersensitivity reaction by binding to serum proteins to form a hapten-carrier complex, which can trigger the production of IgE antibodies. It can also cause type II hypersensitivity reactions by binding to cell surface proteins and triggering complement-mediated lysis or antibody-dependent cell-mediated cytotoxicity. Penicillin can cause type III hypersensitivity reactions by forming immune complexes with penicillin and self-antigens that deposit in tissues and trigger complement activation and inflammation. Finally, penicillin can cause type IV hypersensitivity reactions by inducing a delayed T-cell-mediated response.
17- d) Down Syndrome
Down Syndrome is not an example of a type III hypersensitivity reaction.
Type III hypersensitivity reactions involve the formation of immune complexes between antigens and antibodies, which then deposit in tissues and trigger inflammation and tissue damage.
Systemic Lupus Erythematosus and Rheumatoid Arthritis are both examples of type III hypersensitivity reactions, where autoantibodies bind to self-antigens and form immune complexes that deposit in tissues, leading to chronic inflammation and tissue damage.
Good Pasture’s syndrome is also an example of a type III hypersensitivity reaction, where autoantibodies bind to antigens in the basement membrane of the kidneys and lungs, leading to inflammation and damage to these organs.18- c) Neutrophils and macrophages clear the immune complexes and tissue damage.
Type III hypersensitivity reactions involve the formation of immune complexes between antigens and antibodies, which then deposit in tissues and trigger inflammation and tissue damage.
Systemic Lupus Erythematosus and Rheumatoid Arthritis are both examples of type III hypersensitivity reactions, where autoantibodies bind to self-antigens and form immune complexes that deposit in tissues, leading to chronic inflammation and tissue damage.
Good Pasture’s syndrome is also an example of a type III hypersensitivity reaction, where autoantibodies bind to antigens in the basement membrane of the kidneys and lungs, leading to inflammation and damage to these organs.18- c) Neutrophils and macrophages clear the immune complexes and tissue damage.
19- c) CD8+ T Helper-1 cells are primarily activated after exposure to antigen
During the sensitization phase of DTH, CD4+ T Helper-1 cells are primarily activated after exposure to antigens. These CD4+ T cells recognize and interact with antigens presented on MHC class II molecules on antigen-presenting cells (APCs), leading to their activation and clonal expansion. Activated CD4+ T cells then differentiate into effector cells that secrete cytokines and activate other cells, including macrophages and CD8+ T cells.
CD8+ T cells also play a role in DTH but are primarily involved in the effector phase of the response, where they recognize and kill cells that display antigenic peptides on MHC class I molecules.
Therefore, option (c) "CD8+ T Helper-1 cells are primarily activated after exposure to antigen" is not true regarding the sensitization phase of DTH.
CD8+ T cells also play a role in DTH but are primarily involved in the effector phase of the response, where they recognize and kill cells that display antigenic peptides on MHC class I molecules.
Therefore, option (c) "CD8+ T Helper-1 cells are primarily activated after exposure to antigen" is not true regarding the sensitization phase of DTH.
20- b) T Helper 2 cells secrete antibodies and activate antibody-dependent cell cytotoxicity
During the effector phase of DTH, activated CD4+ T Helper 1 cells secrete cytokines, such as IFN-γ, TNF-α, and IL-2, which activate macrophages and enhance their cytotoxic activity. The macrophages, in turn, phagocytose the antigen and present it to CD4+ T cells, thereby amplifying the immune response. The response generally peaks at 48-72 hours after a second exposure to the antigen. DTH response becomes self-destructive to the intense response that is visible as the granulomatous reaction. T Helper 2 cells, on the other hand, are primarily involved in the humoral immune response and secrete cytokines such as IL-4, IL-5, and IL-13 to promote antibody production and B cell activation. They do not activate antibody-dependent cell cytotoxicity.
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