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MEDLBS 5200 - Immunology > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Describe the difference between a Pathogenic Antigen and an Allergen

A 
Both are molecules capable of inducing an immune response
from pathogen (antigen) vs from non-pathogen (allergen)
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2
Q

Hypersensitivity

A

Exaggerated response to a harmless antigen that results in injury to the tissue, disease, or even death

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3
Q

Characteristics of Type 1 Hypersensitivity

A

IgE, Soluble molecule antigen, IgE induced mast cell activation mechanism, Ex Allergic rhinitis, allergic asthma

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4
Q

Characteristics of Type 2 Hypersensitivity

A

IgG/IgM, Cell associated molecule antigen, Complement mediated phagocytosis mechanism, Ex Chronic urticaria (auto antibodies)

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5
Q

Characteristics of Type 3 Hypersensitivity

A

IgG/IgM, Soluble Molecule, Tissue damage induced by immune complexes mechanism, ex serum sickness, arthus reaction

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6
Q

Characteristics of Type 4 Hypersensitivity

A

T cells, Soluble or cell associated molecule antigen, T cell mediated inflammation or cytotoxicity mechanism, Ex Multiple sclerosis, contact dermatitis, crohn’s disease

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7
Q

How does IgE respond in a Type 1 Hypersensitivity reaction?

A

IgE binds to FcEpsilonR on mast cells and basophils
Cross-linking of Mast Cell IgE with allergen triggers clinical signs of type 1 HS
Characteristic of atopic individuals
1 - IgE immune response to allergen develops-characteristic of atopic individuals
2 - IgE binds to FcEpsilonR on mast cells and basophils
3 - Subsequent allergen exposure results in cross-linking of two+ IgE on surface
4 - Cross-linking triggers immediated release of preformed mediators - Fast (seconds to minutes)
5 - Activated cells also synthesize late mediators (6-8hrs) from membrane phospholipids

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8
Q

What are the phases of type 1 hypersensitivity?

A

Immediate/Initial vs Late phase

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9
Q

What are mediators of type 1 hypersensitivity?

A

Immediate - fast released, preformed mediators (Granule contents - Histamine, Proteases, Chemotatic factors)
Late - synthesized from membrane phospholipids

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10
Q

Anaphylaxis

A

Caused by? systemic release of histamine

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11
Q

Examples of Type 1 Hypersensitivity

A

Rhinitis (pollen), Food allergies (nuts)

- from localized release of histamine in nasal area or GI tract

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12
Q

Skin testing/Patch test Type 1 Hypersensitivity Testing

A
  • Gold standard
  • Inject allergen under skin, wheal and flare develop within 15 minutes in sensitized individuals
    Problems - Variability (site, amount of allergen), severe reaction
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13
Q

Type 1 Hypersensitivity testing

A

In vivo vs in vitro
Vivo - Skin testing/ Patch test
Vitro - RIST/RAST

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14
Q

RIST vs RAST

A

RIST - Radio Immuno Sorbent Test : Measure total IgE

RAST - Radio Allergo Sorbent Test : Measure antigen-specific IgE

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15
Q

RIST results

A 
<2 = Normal in infants = Not allergic 
>10 = high in infants = highly likely allergy 
>/= 100 = Possible allergy = additional testing 
>/= 400 = Abnormally high in adults = Highly likely atopy
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16
Q

Mechanisms of Type 2 Hypersensitivity reactions

A

Killing of target cell by effector-macrophage/NK cell, Complement mediated lysis, Receptor specific autoantibody interferes with signal transduction

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17
Q

type 2 Hypersensitivity examples

A
  • Transfusion reactions
  • Hemolytic disease of the newborn (HDN)
  • Autoimmune hemolytic anemia (including warm and cold autoagglutinins)
  • Goodpasture’ssyndrome
  • Hashimoto’s disease
  • Myasthenia gravis
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18
Q

Hemolytic disease of the newborn

A

appears in infants whose mothers have been exposed to blood-group antigens on the baby’s cells that differ from their own. The mother makes IgG antibodies in response to these antigens that cross the placenta to destroy the fetal RBCs
- Exposure usually occurs during the birth process when fetal cells leak into the mother’s circulation. Typically, the first child is unaffected; however, the second and later children have an increased risk of the disease because of an anamnestic re- sponse

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19
Q

Treatment for severe HDN

A

involves an exchange transfusion to replace antibody-coated RBCs. If serum antibody titrations during the pregnancy in- dicate a high level of circulating antibody, intrauterine trans- fusions can be performed

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20
Q

HDN Prevention

A

To prevent the consequences of HDN, all women should be screened at the onset of pregnancy. If they are Rh-negative, they should be tested for the presence of anti-D antibodies on a monthly basis. In current practice, anti-D immune globulin, called Rhogam, is administered prophylactically at 28 weeks of gestation and within 72 hours following delivery.43 The mecha- nism by which Rhogam works is not completely known, but it is thought to facilitate clearance of the fetal RBCs through opsoniza- tion and therefore suppress production of maternal antibody

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21
Q

type 2 Hypersensitivity tests

A

Direct test (DAT), Coomb’s, Indirect test

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22
Q

characteristics of type 2 hypersensitivity tests

A

DAT - Need baby’s blood, detects in vivo binding of Ig to RBC
Coomb’s - Antiglobulin test (anti-IgG + anti-C3b), Followed by anti-igG alone or anti-C3b alone tests to determine if causative Ig is IgG or IgM
Indirect test - Need mom’s serum, detects ex vivo binding of Ig to RBC

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23
Q

Allergen

A

An antigen that triggers a type I hypersensitivity response

i.e., an allergy

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24
Q

Allergy immunotherapy (AIT)

A

Therapy involving administrationof increasing doses of an allergen over time with the goal of inducing immune tolerance to the allergen

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25
Q

Anaphylaxis

A

A life-threatening response to an allergen characterized by the systemic release of histamine

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26
Q

Arthus reaction

A

A type III hypersensitivity skin reaction that occurs when an animal has a large amount of circulating antibody and is exposed to the antigen intradermally, resulting in localized deposition of immune complexes

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27
Q

Atopy

A

An inherited tendency to respond to naturally occurring allergens; it results in the continual production of IgE

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28
Q

Autoimmune hemolytic anemia

A

An autoimmune disorder in which patients form antibodies that destroy their own red blood cells (RBCs)

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29
Q

Cold agglutinins

A

Antibodies that react below 30°C, typically formed in response to diseases such as Mycoplasma pneumonia and certain viral infections

30
Q

Contact dermatitis

A

A delayed hypersensitivity reaction caused by T-cell sensitization to low molecular weight compounds, such as nickel and rubber, that come in contact with the skin.

31
Q

Delayed hypersensitivity

A

Type IV or T-cell–mediated hypersensitivity; so named because its manifestations are not seen until 24 to 48 hours after exposure to the inducing antigen

32
Q

Direct antiglobulin test (DAT)

A

A technique to determine in vivo attachment of antibody or complement to red blood cells (RBCs), using anti-human globulin to cause a visible agglutination reaction.

33
Q

Granulomas

A

An organized cluster of inflammatory cells formed in some type IV hypersensitivity responses.

34
Q

Hemolytic disease of the newborn (HDN)

A

A cytotoxic reaction that destroys an infant’s red blood cells (RBCs) because of placental transfer of maternal antibodies to Rh antigens

35
Q

Histamine

A

A vasoactive amine released from mast cells and basophils during an allergic reaction

36
Q

Hypersensitivity

A

A heightened state of immune responsiveness

37
Q

Immediate hypersensitivity

A

Reaction to an allergen that occurs in minutes and can be life-threatening

38
Q

Isohemagglutinins

A

Antibody that agglutinates red blood cells (RBCs) of other individuals of the same species

39
Q

Leukotrienes (LT)

A

A class of secondary mediators released from mast cells and basophils during type I hypersensitivity reactions

40
Q

Paroxysmal cold hemoglobinuria

A

A condition in which patients produce a biphasic autoantibody that binds to RBCs at cold temperatures and activates complement at 37°C to produce an intermittent hemolysis

41
Q

Serum Sickness

A

A type III hypersensitivity reaction that results from the buildup of antibodies to animal serum used in passive immunization

42
Q

Type 1 hypersensitivity

A

An allergic reaction in which antigen-specific IgE antibody binds to mast cells and basophils, triggering degranulation and the release of chemical mediators; also known as anaphylactic hypersensitivity

43
Q

Type 2 hypersensitivity

A

An immune reaction in which IgG or IgM antibodies are produced to cell surface receptors, causing damage to the cells, dysfunction of the cells, or overstimulation
of the function of the cells; also known as antibody-mediated cytotoxic hypersensitivity

44
Q

Type 3 hypersensitivity

A

An immune reaction in which IgG or IgM antibodies react with soluble antigens to form small complexes that precipitate in the tissues and activate complement to induce inflammation; also known as complex-mediated hypersensitivity

45
Q

Type 4 hypersensitivity

A

A cell-mediated response involving the release of cytokines that induce inflammation and tissue damage 24 to 72 hours after contact with an antigen

46
Q

Describe the difference between a Pathogenic Antigen and an Allergen

A 
Both are molecules capable of inducing an immune response
from pathogen (antigen) vs from non-pathogen (allergen)
47
Q

Hypersensitivity

A

Exaggerated response to a harmless antigen that results in injury to the tissue, disease, or even death

48
Q

Characteristics of Type 1 Hypersensitivity

A

IgE, Soluble molecule antigen, IgE induced mast cell activation mechanism, Ex Allergic rhinitis, allergic asthma

49
Q

Characteristics of Type 2 Hypersensitivity

A

IgG/IgM, Cell associated molecule antigen, Complement mediated phagocytosis mechanism, Ex Chronic urticaria (auto antibodies)

50
Q

Characteristics of Type 3 Hypersensitivity

A

IgG/IgM, Soluble Molecule, Tissue damage induced by immune complexes mechanism, ex serum sickness, arthus reaction

51
Q

Characteristics of Type 4 Hypersensitivity

A

T cells, Soluble or cell associated molecule antigen, T cell mediated inflammation or cytotoxicity mechanism, Ex Multiple sclerosis, contact dermatitis, crohn’s disease

52
Q

How does IgE respond in a Type 1 Hypersensitivity reaction?

A

IgE binds to FcEpsilonR on mast cells and basophils
Cross-linking of Mast Cell IgE with allergen triggers clinical signs of type 1 HS
Characteristic of atopic individuals
1 - IgE immune response to allergen develops-characteristic of atopic individuals
2 - IgE binds to FcEpsilonR on mast cells and basophils
3 - Subsequent allergen exposure results in cross-linking of two+ IgE on surface
4 - Cross-linking triggers immediated release of preformed mediators - Fast (seconds to minutes)
5 - Activated cells also synthesize late mediators (6-8hrs) from membrane phospholipids

53
Q

What are the phases of type 1 hypersensitivity?

A

Immediate/Initial vs Late phase

54
Q

What are mediators of type 1 hypersensitivity?

A

Immediate - fast released, preformed mediators (Granule contents - Histamine, Proteases, Chemotatic factors)
Late - synthesized from membrane phospholipids

55
Q

Immediate vs delayed Hypersensitivity

A

Immediate (1-3) - symptoms develop within a few minutes to a few hours
Delayed (4) - manifestations are not seen until 24-48 hours after contact with antigen

56
Q

What is the characteristic that all hypersensitivity reactions share

A

all have an aysmptomatic initial phase in which sensitization to Ag occurs

57
Q

Which of the following is a general characteristic of

hypersensitivity reactions?

A

c. An exaggerated immune response to an antigen

58
Q

Which of the following is associated with an increase

in IgE production?

A

b. Activation of Th2 cells

59
Q
  1. Which of the following would cause a positive DAT test?
A

Presence of IgG on RBCs
b. Presence of C3b or C3d on RBCs
c. A transfusion reaction caused by preformed antibody
D. Any of the above

60
Q
  1. All of the following are associated with type I hyper-

sensitivity except

A

a. release of preformed mediators from mast cells.
B. activation of complement.
c. cell-bound antibody bridged by antigen.
d. an inherited tendency to respond to allergens.

61
Q
  1. Which of the following is associated with anaphylaxis?
A

a. Buildup of IgE on mast cells

62
Q
  1. To determine if a patient is allergic to rye grass, the

best test to perform is the

A

b. skin prick test.

63
Q
  1. Which condition would result in HDN?
A

d. Prior exposure to foreign RBC antigen

64
Q
  1. What is the immune mechanism involved in type III

hypersensitivity reactions?

A

b. Deposition of immune complexes occurs in anti-body excess.

65
Q
  1. What is the immune phenomenon associated with the Arthus Reaction?
A

c Deposition of immune complexes in blood vessels

66
Q

10 . Which of the following conculsions can be drawn about a patient whose total IgE level was determined to be 150 IU/ml?

A

Antigen-specific testing should be done

67
Q
  1. Which of the following explains the difference between type 2 and type 3 hypersensitivity reactions?
A

Type 2 involves cellular antigens

68
Q

12 two days after administration of the PPD test, a female health-care worker developed an area of redness and induration 12 mm in size at the injection site. This result means that she has

A

been exposed to M tuberculosis

69
Q
  1. A young woman developed red, itchy papules on her wrist 2 days after wearing a new bracelet. This reaction was caused by
A

an inflammatory response induced by cytokines released from Th1 cells

70
Q
  1. Reactions to latex are caused by
A

type 1 hypersensitivity

71
Q

15 To determine a cold agglutinin titer

A

patien serum should be separated from whole blood at 37c and tested at 4c

MEDLBS 5200 - Immunology (15 decks)

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