Hypersensitivity Flashcards
(123 cards)
1
Q
Type of hypersensitivity with this pathologic immune mechanism:
Th2 cells, IgE, mast cells, eosinophils
A
Immediate hypersensitivity (Type I)
2
Q
Type of hypersensitivity with this pathologic immune mechanism:
IgM, IgG antibodies against cell surface or extracellular matrix antigens
A
Antibody-mediated diseases (Type II)
3
Q
Type of hypersensitivity with this pathologic immune mechanism:
Immune complexes of circulating (soluble) antigens and IgM or IgG deposited in vascular basement membrane
A
Immune complex-mediated diseases (Type III)
4
Q
Type of hypersensitivity with this pathologic immune mechanism:
Cytokine-mediated inflammation (CD4+ T cells)
T-cell mediated killing (CD8+ CTLs)
A
T cell-mediated diseases (Type IV)
5
Q
Type of hypersensitivity with this mechanisms of tissue injury and disease:
Mast cell-derived mediators (vasoactive amines, lipid mediators, cytokines)
Cytokine-mediated inflammation (eosinophils, neutrophils)
A
Immediate hypersensitivity (type I)
6
Q
Type of hypersensitivity with this mechanisms of tissue injury and disease:
Complement and Fc receptor-mediated recruitment and activation of leukocytes (neutrophils, macrophages)
Opsonization and phagocytosis of cells
Abnormalities in cellular function (e.g. hormone receptor signaling)
A
Antibody-mediated diseases (Type II)
7
Q
Type of hypersensitivity with this mechanisms of tissue injury and disease:
Complement and Fc receptor-mediated recruitment and activation of leukocytes
A
Immune complex-mediated diseases (Type III)
8
Q
Type of hypersensitivity with this mechanisms of tissue injury and disease:
Macrophage activation, cytokine-mediated inflammation
Direct target cell lysis, cytokine-mediated inflammation
A
T cell-mediated diseases (Type IV)
9
Q
Allergy responses rely on these being present
A
Antibodies
10
Q
Allergy responses rely on this occurring
A
Cross linking
11
Q
The primary determinant of a vigorous IgE response to an allergen
A
IL-4
12
Q
These cells produce cytokines that tell the B cells to isotype switch to IgE in type I hypersensitivity
A
Th2 cells
13
Q
Fc receptor of IgE
A
FceRI
14
Q
FceRI is a receptor for this
A
IgE
15
Q
These cells degranulate when antigen-specific IgE cross-links its Fc receptor
A
Mast cells
16
Q
Mast cells are different from basophils in that they exist in:
A
Tissues
17
Q
Basophils are different from mast cells in that they exist in:
A
Blood
18
Q
Two similar types of cells that have granules which contain histamine
A
Mast cells and basophils
19
Q
Mast cells possess 50-200 of these which contain effector molecules and are ready for release upon cross-linking of Fc receptor
A
Cytoplasmic granules
20
Q
3 types of products preformed in mast cell granules
A
Enzymes (tryptase, chymase, cethepsin G, carboxypeptidase - remodel connective tissue matrix)
Toxic mediators (histamine, heparin - poison parasites, increase vascular permeability, cause smooth muscle contraction)
Cytokine (TNF-alpha - promotes inflammation, stimulates cytokine production by many cells, activates endothelium)
21
Q
2 toxic mediators preformed in mast cell degranulations
A
Histamine and heparin
22
Q
Cytokine preformed in mast cell granules which promotes inflammation, stimulates cytokine production by many cell types, and activates endothelium
A
TNF-alpha
23
Q
Two cytokines released by mast cells (but not preformed in granules) that stimulate and amplify Th2 response
A
IL-4 and IL-13
24
Q
3 Cytokines released by mast cells (but not preformed in granules) that promote eosinophil production and activation
A
IL-3, IL-5, GM-CSF
25
Chemokine released by mast cells (but not preformed in granules) that attracts monocytes, macrophages, and neutrophils
CCL3
26
Lipid mediators released by mast cells (but not preformed in granules) that cause smooth muscle contraction, increase vascular permeability, and cause mucus secretion
Leukotrienes C4, D4, E4
27
Lipid mediator released by mast cells (but not preformed in granules) that attracts leukocytes, amplified production of lipid mediators, activates neutrophils, eosinophils, and platelets
Platelet-activating factor
28
The following are effects of this type of cell mediators:
Vascular dilation, smooth muscle contraction
Tissue damage
Vascular dilation
Inflammation (leukocyte recruitment)
Mast cell mediators
29
Word for swelling that occurs at site of inoculation with an allergy during skin testing
Wheal
30
Word for redness that occurs at site of inoculation with an allergy during skin testing
Flare
31
This response can be seen within minutes (due to mast cell degranulation) after inoculation with allergen during skin testing
Wheal and flare reaction
32
Subcutaneous allergic reactions are characterized by the raised swelling (wheal) and redness (flare) that occur at the site within 20 minutes of intradermal exposure, and effects are mediated by this
Histamine
(mast cell degranulation)
33
Immediate or late phase reactions are IgE mediated and part of type I response?
Both
34
Late-phase reaction during skin allergen testing occur due to these 3 things synthesized by mast cells after the immediate phase of the response
Leukotrienes
Chemokines
Cytokines
35
This part of the wheal-and-flare reaction is caused by edema resulting from the histamine-induced capillary permeability
Wheal
36
This part of the wheal-and-flare reaction is caused by vasodilation and increased blood flow
Flare
37
Does vasodilation or vasoconstriction occur during type I hypersensitivity?
Vasodilation
Causes flare (redness)
38
Treatment of type I hypersensitivities focus on blocking the effects of these
Inflammatory mediators
(e.g. drugs that inhibit histamine and leukotrienes)
39
Food allergens are associated with localized _____ release that leads to diffusion of Ag into blood vessels
This can lead to smooth muscle contraction that induces vomiting and diarrhea
When a food or drug allergen gets carried to the skin within the bloodstream, urticaria and angioedema can develop (in some cases as precursors to systemic anaphylaxis)
Histamine
40
Allergic reactions in the lung involve recruitment of these cells which are not typically present in healthy tissue
Eosinophils
41
This stimulates the reformation of tight junctions between endothelial cells, reducing permeability and preventing fluid loss from blood, which diminishes tissue swelling and raises blood pressure
Also relaxes constricted bronchial smooth muscle and stimulates the heart
Epinephrine
42
This is almost always the treatment for anaphylactic shock
Epinephrine
43
Fall in blood pressure (shock) caused by vascular dilation; airway obstruction due to laryngeal edema and bronchial construction
Almost always treated with epinephrine
Anaphylaxis
44
Activated mast cells secrete this, which induces eosinophil production from bone marrow
IL-5
45
Activated mast cells secrete IL-5, which induces bone marrow to produce these cells
Eosinophils
46
These 4 chemokines interact with CCR3 receptor expressed by eosinophils to attract them to site of allergen exposure
CCL5, CCL7, CCL11, and CCL13
47
chemokines CCL5, CCL7, CCL11, and CCL13 interact with this on eosinophils to attract them to site of allergen exposure
CCR3 receptor
48
What is the role of CCR3 receptor?
Is on eosinophils and interacts with CCL5, CCL7, CCL11, and CCL13 to attract them to site of allergen exposure
49
The most important chemokine for eosinophils, is produced by activated endothelial cells, T cells, and monocytes
CCL11 (eotaxin)
50
3 types of cells that produce CCL11 (eotaxin)
Activated endothelial cells, T cells, and monocytes
51
What is the role of CCL11?
is an eotoxin
the most important chemokine for eosinophils
52
Unlike mast cells, resting eosinophils do not express this on their surface, and thus do not naturally coat themselves with IgE
FceRI
53
The presence of these cells is typically associated with chronic allergic inflammation (e.g. chronic asthma)
Eosinophils
54
Enzymes and toxic proteins released by ______ have the potential to induce more damage than those released from mast cells
Eosinophils
55
Enzymes and toxic proteins released by eosinophils have the potential to induce more damage than those released from ______
Mast cells
56
3 cytokines that amplify eosinophil by bone marrow and cause eosinophil activation
IL-3, IL-5, GM-CSF
57
Lipid mediators that cause smooth muscle contraction, increase vascular permeability, and cause mucus secretion
Are produced by eosinophils but not preformed in granules
Leukotrienes C4, D4, E4
58
In chronic responses, these two types of cells help activate the eosinophils to cause tissue damage, recruitment of inflammatory cells (i.e. neutrophils), and irreversible damage to the airways, all of which are characteristic of chronic asthma
Mast cells and Th2 cells
59
Chronic asthma can develop into this type of hypersensitivity
Type IV
60
What is the difference between chronic asthma and allergic asthma?
Chronic asthma involves a hyper-responsiveness and hyper-reactivity of the airways, and exposure to the allergen is no longer needed to initiate an asthma attack
61
Chronic asthma primarily involves this type of cell
Th2 cells
IgE is no longer the immune reactant
62
Therapy for anaphylaxis that causes vascular smooth muscle contraction, increases cardiac output (to counter shock), and inhibits bronchial smooth muscle cell contraction
Epinephrine
63
Treatment for asthma that reduces inflammation
Corticosteroids
64
Treatment for asthma that relaxes bronchial smooth muscle and reduces inflammation
Leukotriene antagonists
65
Repeated administration of low doses of allergens as treatment for allergic diseases
Desensitization
66
Treatment for allergic diseases that block actions of histamine on vessels and smooth muscles
Antihistamines
67
Treatment for allergic diseases that inhibits mast cell degranulation by stabilizing their membrane (blocks the release of histamine)
Cromolyn
68
Difference between antihistamines and cromolyn
Antihistamines block actions of histamine on vessels and smooth muscles
Cromolyn inhibits mast cell degranulation and thus blocks the release of histamine
69
Corticosteroid therapy reduces these 5 molecules
Cytokines
NOS
Prostaglandins
Leukotrienes
Adhesion molecules
70
While corticosteroid therapy reduces cytokines (reducing inflammation), NO, decreases prostaglandin and leukotrienes, and adhesion molecules, it results in the induction of these as well, leading to induction of apoptosis in lymphocytes and eosinophils
Endonucleases
71
Desensitization involves repeated administration of low doses of Ag in an attempt to drive immunity in this direction
Away from IgE and toward IgG
72
Penicillin binding to this leads to an opening of the beta-lactam ring, which forms a covalent bond with a residue in the active site, thus inactivating the enzyme
Bacterial transpeptidase
73
Penicillin is an example of a hapten-carrier system, meaning?
Penicillin becomes immunogenic when it binds to carrier proteins
Penicillin combines with the erythrocyte surface, acting as a hapten. This induces an antibody response directed against the penicillin-coated erythrocyte membrane.
74
Penicillin binding to bacterial transpeptidase leads to an opening of this, which forms a covalent bond with a residue in the active site of the transpeptidase, thus inactivating the enzyme
Beta-lactam ring
75
Penicillin-reactive antibodies can be either of these
IgE or IgG
This can lead to type I, II, or III hypersensitivity
76
Type II hypersensitivities are mediated by _____ that is directed toward cell surface antigens
IgG
77
In type II hypersensitivity to penicillin, complement-coated penicillin-modified ______ are phagocytosed by macrophages using their complement receptor
Erythrocytes cells
Macrophages then present peptides to CD4 T cells, which become Th2 cells that activate B cells to become plasma cells secreting IgG
78
ABO blood group antigens are this type of hypersensitivity
Type II
79
ABO blood group antigens are ______ that coat erythrocytes
Glycolipids
80
ABO blood group antigens are glycolipids that coat these
Erythrocytes
81
Hemolytic disease of the newborn is an example of this type of hypersensitivity
Type II
82
Type III hypersensitivity involves IgG toward ____ antigens
soluble
83
During a type III hypersensitivity, binding of immune complex to this on mast cell induces degranulation
FcyRIII
84
Arthus reaction involves local inflammation, increased fluid and protein release, and blood vessel occlusion, and is an example of this type of hypersensitivity
Type III
85
In Arthus reaction (type III hypersensitivity), accumulation of these leads to complement fixation
Immune complexes
86
In Arthus reaction (type III hypersensitivity), accumulation of immune complexes leads to this
Complement fixation
87
The Arthus reaction (type III hypersensitivity) is associated with these antibodies
IgG (not IgE)
but it involves mast cell degranulation (FcyRIII receptors)
88
This is common at the site of injection of individuals receiving inoculations for desensitization (induced IgG reacts with mast cells and injection site)
Arthus reaction
89
Hemorrhaging in the skin and urticarial rashes can develop during these hypersensitivity reactions
Type III
90
Serum sickness is this type of hypersensitivity
Type III
91
Type of type III hypersensitivity involving passive transfer of antibodies from a different species used to treat infections
Immune response toward antibodies from foreign species
Serum sickness
Today, antivenin and IVIG represent common sources of serum sickness
92
Antivenin and IVIG represent common sources of this
Serum sickness
93
Type of Type IV hypersensitivity reaction:
Insect venom and mycobacterial proteins can be antigens
Leads to local skin swelling (erythema, induration, cellular infiltrate, dermatitis)
Delayed-type hypersensitivity
94
Type of Type IV hypersensitivity reaction:
Pentadecacatechol (poison ivy), DNFB, and small metal ions (nickel, chromate) can be antigens
Leads to local epidermal reaction (erythema, cellular infiltrate, vesicles, intraepidermal abscesses)
Contact hypersensitivity
95
Type of Type IV hypersensitivity reaction:
Gliadin can be antigen
Leads to villous atrophy in small bowel, malabsorption
Gluten-sensitivity enteropathy (celiac disease)
96
Delayed-type hypersensitivity is this type of hypersensitivity
Type IV
97
Contact hypersensitivity is this type of hypersensitivity
Type IV
98
Gluten-sensitivity enteropathy (celiac disease) is this type of hypersensitivity
Type IV
99
Delayed type hypersensitivity takes this long to peak
2-3 days
Instead of minutes-to-hours like the other hypersensitivities
100
Type of hypersensitivity that takes 2-3 days to peak and require 100-1000 times more Ag than others
Delayed type hypersensitivity (type IV)
101
Delayed type hypersensitivity primarily involves this type of cell
Th1
102
In a delayed type hypersensitivity, Th1 cells release this, which activates macrophages, increasing release of inflammatory mediators
IFN gamma
103
In a delayed type hypersensitivity, Th1 cells release these, which lead to local tissue destruction and increased expression of adhesion molecules on local blood vessels
TNF-a and LT
104
In a delayed type hypersensitivity, Th1 cells release these, which leads to monocyte production by bone marrow stem cells
IL-3 and GM-CSF
105
Delayed type hypersensitivity can involve these 2 antigens
Insect venom
Mycobacterial proteins (tuberculin, lepromin)
106
Contact hypersensitivity can involves these 3 antigens
Pentadecacatechol (poison ivy)
DNFB
Small metal ions (nickel, chromate)
107
Contact hypersensitivity to poison ivy can be induced by physical contact with this
The hapten pentadecacatechol
108
In Contact hypersensitivity, the hapten pentadecacatechol forms a covalent bond with these
Extracellular matrix proteins
109
Dendritic cells in the skin
Langerhans cells
110
Contact hypersensitivity can occur with bivalent nickel ions that chelated by this in human proteins
Histidine
111
Contact hypersensitivity due to poison ivy can lead to the activation of these 2 types of cells
Th1 cells (via MHC II)
CD8 T cells (when pentadecacatechol crosses the plasma membrane and chemically modified intracellular protein, leading to MHC I presentation)
112
There is a strong genetic predisposition to celiac disease, and it has been tracked molecularly to transglutaminase modification of this
Glutamine (Q) residues to glutamate (E)
113
In Celiac disease, there is peptide loaded onto either of these
HLA-DQ2 or HLA-DQ8
114
In Celiac disease, peptide is loaded onto HLA-DQ2 or HLA-DQ8, and effector T cells of this lineage
Th1
115
All celiacs make these types of antibodies toward tissue transglutaminase, and many make anti-gliadin antibodies
IgG or IgA
116
All celiacs make IgG or IgA toward this
Tissue transglutaminase
117
All celiacs make IgG or IgA toward tissue transglutaminase, and many also make antibodies to this as well
Anti-gliadin antibodies
118
Type of reaction to penicillin that involves urticaria and systemic anaphylaxis
Type I (IgE)
119
Type of reaction to penicillin that involves hemolytic anemia
Type II (IgM, IgG)
120
Type of reaction to penicillin that involves serum sickness and glomerulonephritis
Type III (IgG)
121
Type of reaction to penicillin that involves contact dermatitis
Type IV (Tdth cells)
122
Type IV hypersensitivity that involves macrophage activation and is seen in contact dermatitis or tuberculin reaction, utilizes these type of T cells
Th1 cells
123
Type IV hypersensitivity that involves eosinophil activation and is seen in chronic asthma and chronic allergic rhinitis, utilizes these types of T cells
Th2 cells
