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Immuno Exam 3 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What are the functions of IL-4

A
  • induce differentiation of Th2 cells

- cause class switching to IgE

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2
Q

What receptor does IgE bind to on mast cells, basophils and activated eosinophils?

A

FceRI

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3
Q

How is IgE synthesized?

A

IgE is synthesized from class switching

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4
Q

IgE has how many constant domains

A

2

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5
Q

IgE does not play a role in

A. Complement fixation 
B. Opsonization 
C. Allergic Reactions
D. Defense against parasitic worms
E. A & B
F C & D
A

E

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6
Q

When is IgE synthesized?

A

When Th2 cells secrete IL-4 which stimulates B cells to class switch and secrete IgE

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7
Q

How does the adaptive immune system play a role in parasitic infections

A

Th2 cells secrete IL-4 to induce the differentiation of more Th2 cells and class switching of B cells to make IgE

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8
Q

What happens to IgE once it is synthesized

A

it diffuses across vessel endothelium out of the blood to bind to mast cells

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9
Q

T/F: FceRII is a high affinity receptor for IgE

A

False

*FceRI

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10
Q

What chain of the FceRI receptor binds IgE

A

the alpha chain

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11
Q

The _____ chain of FceRI binds IgE

A

Alpha

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12
Q

Mast cells are located in all of the following locations except

A. Tissue Lining
B. Vascularized Tissue
C. Mucosal Tissue 
D. Blood
E. Connective Tissue
A

D. Blood

*basophils are located in in the blood

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13
Q

Mast cells are ____ lived while basophils are ____ lived

A

Short, long

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14
Q

Mast cells in mucosal tissue express which protease

A

Tryptase

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15
Q

Mast cells in connective tissue express which protease?

A

ChymoTryptase

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16
Q

-

A

-

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17
Q

Which granulocyte is mainly present in blood?

A

Basophils

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18
Q

_______ on mast cells and basophils secrete cytokines that result in Th2 response and eosinophil activation

A

Toll Like receptors

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19
Q

Which cytokine is responsible for Eosinophil production and activation

A

IL-5

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20
Q

Eosinophils are mainly located

A. in blood
B. in tissue linings
C. in lymph
D. in connective tissues

A

D

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21
Q

What structures on basophils and mast cells recognize features of pathogens

A

Toll Like Receptors

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22
Q

What is the role of IL-5 in the development of immunity against parasites

A

eosinophil production and activation

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23
Q

List the type of preformed mast cell mediators (3)

A
  • enzyme
  • toxic mediator
  • cytokine
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24
Q

What are the enzymatic preformed mediators of mast cells?

A

-tryptase and and chymotryptase

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25
Q

What do the mast cell enzymatic preformed mediators do?

A

remodel the ECM of tissue to dislodge parasite

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26
Q

What are the toxic preformed mediators of mast cells?

A

Histamine and Heparin and serotonin

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27
Q

What is the main effect of the release of histamine from mast cells?

A

-increased blood flow triggering inflammation

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28
Q

Where are H1 receptors for histamine located? What are the effects at each location?

A

-Vascular endothelial cells: vasodilation (increased permeability)
-Smooth Muscle cells: bronchoconstriction
Heart & Brain

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29
Q

H1 histamine receptors are located everywhere except

A. vascular endothelium
B. GI tract
C. Smooth Muscle
D. Heart
E. Brain
A

B.

*H2 receptors are in the GI and vascular endothelium

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30
Q

Where are H2 receptors located?

A

Vascular endothelium and GI

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31
Q

H3 and H4 receptors are located

A

in CNS and bone marrow

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32
Q

Which cytokine is a preformed mediator secreted by mast cells?

A

TNF-alpha

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33
Q

What does the preformed mediator TNF-alpha do (3)

A
  • promotes inflammation
  • stimulates cytokine production
  • activates endothelium to express adhesion molecules
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34
Q

What is the importance of endothelial cell activation upon TNF-alpha

A

It causes the cells to express adhesion molecules allowing other immune cells to enter the tissue

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35
Q

What are the categories of newly synthesized mast cell mediators (3)

A
  • cytokines
  • chemokines
  • lipid mediators
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36
Q

IL-4 and IL-13 from mast cells are _______ mediators

*chart on slide 13

A

Newly synthesized

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37
Q

What do newly synthesized mast cell mediators cause?

A

Sustained effects (late phase reaction)

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38
Q

Which category of mast cell mediators are responsible for the late phase reaction

A

newly synthesized

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39
Q

What chemokine plays a role in mast cel newly synthesized mediators?

A

CCL3

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40
Q

What does CCL3 do in mast cell mediation

A

Attracts monocytes, macrophages and neutrophils

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41
Q

What cytokine(s) promotes eosinophil production and activation

A

IL-5 & IL-3

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42
Q

What cytokines are a newly synthesized mast cell mediator the stimulates and amplifies the Th2 response

A

IL-4 and IL-13

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43
Q

What do prostaglandins do? (3)

A
  • cause smooth muscle contraction
  • increase vascular permeability
  • cause mucus secretion
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44
Q

How are leukotrienes formed?

A

When arachidonic acid goes through the lipogenase pathway

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45
Q

Which pathway does arachidonic acid undergo to form prostaglandins?

A

Cyclooxygenase paths

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46
Q

T/F: Leukotrienes and Prostaglandins can be blocked by aspirin

A

False

*only Prostaglandins

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47
Q

Eosinophils are resident in

A

-connective tissue under respiratory GI and urogenital tracts

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48
Q

Which of the following cells types are exclusively involved in the late phase reaction

A. Basophils
B. Mast Cells
C. Eosinophils

A

C

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49
Q

Highly toxic mediators of eosinophils

A. amplify inflammatory response
B. directly kill
C. Recruit Mast Cells

50
Q

What are the preformed mediators of eosinophils

A
  • eosinophil peroxidase
  • Major Basic Protein
  • Eosinophil Cationic Protein

*slide 17

51
Q

Leukotirenes and Prostaglandis are

A. Toxic protein
B. Chemokines
C. Lipid Mediator

52
Q

Why are parasites more difficult to eradicate?

A

they are too big to be engulfed by phagocytes and they are biologically and chemically more like humans than other pathogens so they are less antigenic

53
Q

Why are mast cells more versatile than B cell in term of their response to antigen in the context of IgE

A

Mast cells bind to different IgE molecules with various specificities for antigens that can be diverse in the structural and biological origin

54
Q

How do IgE participate in protective immunity against parasites?

A

when IgE crosslinks on mast cell it activates mast cell degranulation which results in the release of toxic proteins to the parasite

55
Q

Define allergy

A

a damaging immune response to harmless agents

56
Q

Describe the hygiene hypothesis

A

Access to hygiene, vaccines and antibiotics relate to low levels of parasitic infections.
Areas with high parasitic infection rates happen to have low levels of allergies while clean areas with low parasitic infection rates tend to have HIGH allergies

57
Q

List the factors that can predispose a person to type 1 hypersensitivity

A

Genetic & Environmental Factors:

  • MHC class II genes
  • TCR alpha locus
  • IL-4
58
Q

What are the 4 types of hypersensitivity

A

Immediate
Cytotoxic
Immune Complex
Delayed Type

59
Q

What are hypersenisitities classified by

A

The mechanisms by which they operate

60
Q

All of the following types of hypersensitivity are mediated by antibodies except

A. Immediate
B. Delayed Type
C. Cytotoxic
D. Immune complex

A

B.

*delayed type is type IV mediated by T cells

61
Q

Hypersensitivity reactions occur when

A

an already immune or sensitized person is re-exposed to the initiating allergen

62
Q

Which types of hyperactivity is mediated by antibodies

A

Type 1: immediate
Type 2: cytotoxic
Type 3: Immune complex

63
Q

T/F: Antibodies are involved in type 4 hypersensitivity

64
Q

What are allergens

A

protein antigens that trigger allergies that resemble parasite antigen

65
Q

How can MHC II genes predispose someone to allergies?

A

It can cause enhanced presentation of particular antigen, having a stronger hold for that antigen

66
Q

How can TCR alpha locus predispose someone to allergies?

A

it can cause enhanced T cell recognition of allergen derived peptides

67
Q

How can IL-4 gene predispose someone to allergies

A

It can cause a variation in expression of IL-4, making them more likely to have Type 1 hypersensitivity response since more IgE is made

68
Q

What are the three stages of Type I hypersensitivity reactions?

A

Sensitization
Immediate Rxn
Late Phase Rxn

69
Q

Describe how a person be come sensitized to type I hypersensitivity?

A
  1. A person is exposed to allergen for the first time
  2. Antigen is extracted and T cells are activated upon being presented with antigen via APC
  3. Th2 cells secrete IL-4 to stimulate class switching in B cells to make IgM
  4. IgM binds to mast cells (* the mast cells are now ready for the next time allergen enters)
    * slide 33
70
Q

What triggers mast cells to degranulate?

A

Crosslinking of IgE due to presence of allergen

71
Q

What preformed mediators are active in the immediate reaction of type I hypersensitivity (3)

A
  • histamine
  • serotonin
  • neutrophil/eosinophil chemotactic factor
72
Q

What mediators are released during the late phase reaction of type 1 hypersensitivity

A
  • leukotrienes

- prostaglandins

73
Q

Why is type 1 hypersensitivity referred to as immediate?

A

Signs and symptoms can occur in minutes after exposure

74
Q

What are the consequences of mast cell degranulation?

A

When mast cell degranulates its releases mediators causing symptoms such as redness, swelling, and smooth muscle contraction. Mast cell also releases arachidonic acid to disrupt membranes

75
Q

What are the 2 main roles of eosinophils?

A
  1. release toxic granular proteins that cause tissue injury

2. amplify inflammatory response by releasing chemokine, prostaglandins and leukotrienes

76
Q

Prostaglandins and leukotrienes present in _____ phase reaction

77
Q

How does ingestion of an allergen influence clinical presentation of type 1 hypersensitivity

A

-expulsion of GI tract contents (diarrhea & vomiting)

78
Q

How does inhalation of an allergen influence clinical presentation of type 1 hypersensitivity

A

Expulsion of airway contents via coughing, sneezing, expulsion of phlegm

79
Q

How does injection of an allergen influence clinical presentation of type 1 hypersensitivity

A

Edema and inflammation, increased flow of antigens in lymph to lymph nodes

80
Q

Allergens in the blood trigger

A

systemic anaphylaxis

81
Q

What symptoms are caused by anaphylactic shock (5)

*think about the effects of type 1 sensitivity in the different regions in the body and what occurs when allergens reach those areas but think of it on a larger scale for systemic anaphylaxis

A 
Itchy rash
nausea/vomiting
drop in BP
difficult breathing
organ damage
82
Q

Describe the process leading up to anaphylactic shock

A

antigen in bloodstream enters tissue and activates mast cells throughout body

mast cell degranulation causes the release of mediators that affect the : heart, respiratory tract and GI tract

83
Q

What effects do inflammatory mediators have on vascular system (4)

A
  • capillary permeability and entry of fluid into tissues
  • edema
  • loss of blood pressure
  • reduced oxygen to tissues
84
Q

What effects do inflammatory mediators have on respiratory system

A
  • contraction of smooth muscles of airways

- difficult swallowing and breathing

85
Q

What effects do inflammatory mediators have on gastrointestinal system

A
  • contraction of smooth muscle

- vomiting

86
Q

Describe how penicillin can cause systemic anaphylaxis

A

Penicillin is a hapten, when it binds to a RBC it is big enough to be recognized and ingested by macrophages. Macrophages present penicillin antigen to T cells which activate B cells to make IgE resulting in an immune response

87
Q

Inhaled allergens in the ______ respiratory tract cause allergic rhinitis

88
Q

Inhaled allergens in the ______ respiratory tract cause asthma

89
Q

What are the acute responses of the immune system in the case of asthma

A
  • mucosal mast cell captures antigen

- mediators cause smooth muscle contraction, mucous production, increased blood vessel permeability

90
Q

Chronic response in asthma is mediated by _____ and _____ products

A

cytokines , eosinophil

91
Q

What are the treatments for type I allergies (3)

A
  • prevention
  • pharmacologic
  • immunologic
92
Q

What is Zolair?

A

Antibodies against IgE that can be administered as intervention to type I allergies

93
Q

What is Mepolizumab?

A

Administered antibodies against IL-5

*stopping eosinophil production and activation

94
Q

Administering antibodies against IL-5 would have what effect

A

It would stop the production and activation of eosinophils thus reducing the late response of Type 1 hypersensitivity

95
Q

______ cells : early response:: eosinophils: late response

96
Q

What are isohemagglutinis?

A

IgM antibodies directed against blood group antigen

97
Q

What is D antigen?

A

The antigen that determines if a person is Rh+ or RH-

98
Q

Which of the following are correctly matched

A. Type 1: Immune complex Hyper sensitivity

B. Type 2: cytotoxic effects

C. Type III: T cell mediated

99
Q

Describe the immune complexes formed in the Arthus Reaction

*slide 61

A

IgG reacts with and forms complexes with soluble proteins that activate complement

100
Q

What are the key mediators in Type 3 hypersensitivity

A

Anaphylatoxins

Chemotaxins

101
Q

C3a and C5a are anaphylatoxins & chemotaxins that cause

A

edema (increased vascular permeability) and tissue damage (influx of neutrophils and platelets)

102
Q

Cytotoxic destruction of a cell in type 2 hypersensitivity is by what mechanisms (3)

A

complement
opsonization
ADCC

103
Q

A person who is blood type A has what type of isohemagglutinin?

A

Anti B antibodies

104
Q

What causes agglutination

A

Antibodies bind to RBCs and crosslink causing the cells to come together

105
Q

What is the main difference between IgM and IgG

A

IgM cant cross placenta

106
Q

What happens in 2nd pregnancy of mom who is Rh- with Rh+ baby

A

IgG crosses placenta and enters fetal circulation and binds to fetal rbc

107
Q

Treatment for hemolytic disease of newborn

A

RhoGam: anti Rhd antibodies—IgG against Rhd antigen is distributed.
It binds to antigen on fetal cells and destroys the hemoglobin

108
Q

What is the immediate result of the formation of immune complexes

A

Complement activation

109
Q

What is the main presentation/characteristic of Type 4 hypersensitivity

A

Erythema and induration due to macrophages and T cells being recruited to area in skin

110
Q

What type compounds trigger contact dermatitis

111
Q

What are the cytokine mediators of Type IV hypersensitivity reactions

A

IFN gamma
TNF beta
monocyte/macrophage chemotactic factor

112
Q

Induration and erythema is the classic halmark associated with

A. Type I
B. Type II
C. Type III
D. Type IV

113
Q

What cell types are involved in type I hypersensitivity

A

Mast cells, basophils, eosinophils

114
Q

What antibody class is involved in type I hypersensitivity?

115
Q

What antibody class is involved in type II hypersensitivity?

116
Q

What antibody class is involved in type III hypersensitivity?

117
Q

What antibody class is involved in type IV hypersensitivity?

118
Q

What mechanism is associated with type II hypersensitivity?

A

Complement / opsonization

119
Q

What mechanism is associated with type III hypersensitivity?

A

Complement and accumulation of neutrophils and platelets

120
Q

What mechanism is associated with type IV hypersensitivity?

A

Th1/ CD8T cells

121
Q

How does local type III hypersensitivity differ from systemic?

A

Local: immune complexes stay local and complement is activates there

Systemic: immune complexes are distributed throughout the body

Immuno Exam 3 (5 decks)

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