Lecture 28 - 29 (Type I & II Hypersensitivity) Flashcards

1
Q

what is hypersensitivity?

A

a state of altered reactivity in which the body reacts with an exaggerated immune response to what is perceived as a foreign substance

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2
Q

hypersensitivity is a reflection of ____________ or ___________ immune responses

A

excessive or aberrant

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3
Q

*Immune Reactant: IgE
*Important Cells Involved: Mast cells (& eosinophils)
*Mechanism of Damage: TH2 response, degranulation of mast cells & eosinophils; inflammation
which hypersensitivity?

A

type I hypersensitivity

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4
Q

*Immune Reactant: IgG (& IgM)
*Important Cells Involved: Neutrophils, Macrophages
*Mechanism of Damage: Antibodies made against cell surface antigens or extracellular matrix antigens; opsonization, phagocytosis, etc.
which hypersensitivity?

A

type II hypersensitivity

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5
Q

*Immune Reactant: IgG (&IgM)
*Important Cells Involved: Neutrophils & Mast Cells
*Mechanism of Damage: Immune complexes of antigen and antibody aren’t removed by phagocytosis; deposited in vascular basement membranes, etc.
which hypersensitivity?

A

type III hypersensitivity

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6
Q

*Immune Reactant: TH1 & CTLs
*Important Cells Involved: T Cells, APCs, Macrophages
*Mechanism of Damage: CD4+ activating macrophages and producing cytokine-mediated inflammation or CD8+ causing direct target cell lysis
which hypersensitivity?

A

type IV hypersensitivity

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7
Q

which hypersensitivity is exemplified by all of the following:

-allergic rhinitis
-food allergies
-bronchial asthma
-systemic anaphylaxis
-vaccine reactions

A

type I hypersensitivity

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8
Q

which hypersensitivity is exemplified by all of the following:

-Immune Mediated Hemolytic Anemia (IMHA)
-Immune Thrombocytopenia (ITP)
-Hemolytic Disease of the Newborn (HDN)
-Myasthenia Gravis
-pemphigus vulgaris
-drug reactions
-Acute Rheumatic Fever

A

type II hypersensitivity

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9
Q

which hypersensitivity is exemplified by all of the following:

-Systemic Lupus Erythematosus (SLE)
-Purpura (Little bruises on the skin)
-Recurrent Airway Obstruction (RAO)
-Blue Eye
-Farmer’s Lung (Hypersensitivity Pneumonitis)
-serum sickness
-Rheumatoid arthritis (Non-Erosive)
-Glomerulonephritis associated with Rheumatic Fever

A

type III hypersensitivity

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10
Q

what cells are responsible for the acute inflammatory response in the early phase of type 1 hypersensitivity?

a. pre-formed Mast Cells
b. T cells (Like TH17)
c. neutrophils & macrophages

A

a. pre-formed Mast Cells

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11
Q

which hypersensitivity is exemplified by all of the following:

-allergic contact dermatitis
-Tuberculin reaction (used for Tb test)
-type 1 diabetes
-erosive arthritis
-Multiple sclerosis

A

type IV hypersensitivity

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12
Q

exaggerated TH2 response & exaggerated IgE production are characteristic of which hypersensitivity?

A

type I hypersensitivity

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13
Q

what cells are responsible for the second wave late phase reaction in a type 1 hypersensitivity 6-12 hours post exposure? (characterized by redness, edema, pruritus)

a. pre-formed Mast Cells
b. T cells (Like TH17)
c. neutrophils & macrophages

A

b. T cells (Like TH17)
c. neutrophils & macrophages

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14
Q

type I hypersensitivity:
binding of antigens with mast cell-bound IgE leads to…

A

mast cell degranulation

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15
Q

the exaggerated TH2 response & exaggerated IgE production seen in Type 1 Hypersensitivity is called:

A

atopy

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16
Q

what is type I hypersensitivity?

A

a form of acute inflammation that results from the interaction of antigens with mast cell-bound IgE

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17
Q

t/f: granule content causes acute inflammation

A

true

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18
Q

immediate hypersensitivity

a) type I hypersensitivity
b) type II hypersensitivity
c) type III hypersensitivity
d) type IV hypersensitivity

A

a) type I hypersensitivity

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18
Q

immune complex-mediated hypersensitivity

a) type I hypersensitivity
b) type II hypersensitivity
c) type III hypersensitivity
d) type IV hypersensitivity

A

c) type III hypersensitivity

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19
Q

antibody-mediated hypersensitivity

a) type I hypersensitivity
b) type II hypersensitivity
c) type III hypersensitivity
d) type IV hypersensitivity

A

b) type II hypersensitivity

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20
Q

T-cell mediated hypersensitivity

a) type I hypersensitivity
b) type II hypersensitivity
c) type III hypersensitivity
d) type IV hypersensitivity

A

d) type IV hypersensitivity

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21
Q

development of atopy and type I hypersensitivity depends upon the interaction of…

A

genes and environmental factors

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21
Q

excessive production of IgE is called __________ and affected individuals are said to be ____________

A

atopy; atopic

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22
Q

what are the two important features of type I hypersensitivity?

A

-exaggerated TH2 response
-excessive IgE production

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23
what is the role of IL-4 in an IgE response such as in type 1 hypersensitivity reactions? a) produced by TH1; promotes more TH1; promotes IgE b) produced by TH2; promotes more TH2; promotes IgE c) produced by TH1; promotes more TH1; inhibits IgE d) produced by TH2: promotes more TH2; inhibits IgE
b) produced by TH2; promotes more TH2; promotes IgE
24
which of the following inhibit IL-44? 1. IFNα/β or IFNγ? 2. IL-2 or IL-12?
1. IFNγ 2. IL-12
25
what is Il-4 produced by?
TH2 cells
26
type I hypersensitivity: once IL-4 is produced by TH2 cells, it promotes the development of more TH2 cells and promotes ______ responses
IgE
27
the response to IL-4 is inhibited by _________ and __________
IFNγ and IL-12
28
what causes degranulation upon a second exposure to allergen? a) co-stimulation by B7 to stimulate mast cells b) cross binding of allergen by IgE bound to mast cells
b) cross binding of allergen by IgE bound to mast cells
28
IgE binds to what on mast cells? a) CD152 b) Fas c) FcεRI receptor d) TLR
c) FcεRI receptor
29
the allergy loop: dendritic cells express trimeric ____________ and as a result can bind antigen-IgE complexes *this antigen, once processed, stimulates TH2 responses and promotes the IgE response
FcεRI receptor
30
what is stimulated to cause the switch to IgE in the first exposure to an allergen? a) TH1 cells b) TH2 cells c) TH17 cells d) Treg cells
b) TH2 cells
31
IgE is associated with rapid degranulation. Which immunoglobulin is associated with normal gradual degranulation?
IgG
32
stimulation of α adrenergic receptors causes: -[enhanced/suppressed] degranulation of mast cells -[contraction/relaxation] of smooth muscle -[constriction/dilation] of blood vessels
-enhanced degranulations of mast cells -contraction of smooth muscles -constriction of blood vessels
33
stimulation of β adrenergic receptors causes: -[enhanced/suppressed] degranulation of mast cells -[contraction/relaxation] of smooth muscle -[constriction/dilation] of blood vessels
-suppressed degranulation of mast cells -relaxation of smooth muscles -dilation of blood vessels
34
to treat allergic reactions by reducing edema and raising blood pressure we use: a) α agonist b) β agonists
a) α agonist
35
36
37
epinephrine (or adrenaline) has both _____ and _____ adrenergic activity
α and β
38
Epinephrine has... a) α adrenergic activity b) β adrenergic activity c) both α & β adrenergic activity d) neither α or β adrenergic activity
c) both α & β adrenergic activity
38
what is the interleukin for eosinophils?
IL-5
39
______________ exacerbate the inflammation triggered first by mast cells via a complex array of molecules that contribute to the acute inflammatory response
eosinophils
40
clinical signs of type I hypersensitivity result from abrupt and excessive release of inflammatory mediators from...
mast cells, basophils, and eosinophils
40
type I hypersensitivity: if the rate of release of vasoactive molecules exceeds its ability to adjust changes in the vascular system, an animal will undergo ________ ___________ and may die
allergic anaphylaxis
40
severe urticaria a) type I hypersensitivity b) type II hypersensitivity c) type III hypersensitivity d) type IV hypersensitivity
a) type I hypersensitivity
41
what is the shock organ in dogs?
hepatic veins (the liver)
42
treatments of type I hypersensitivity (4)
-prevent exposure to the offending allergens -epinephrine for allergic anaphylaxis -corticosteroids for local inflammation -desensitizing injections of allergens
43
for local inflammation we use: a) corticosteroids b) epinephrine
a) corticosteroids
44
for anaphylaxis/systemic type 1 we use: a) corticosteroids b) epinephrine
b) epinephrine
45
what is the shock organ of most animals other than the dog?
respiratory tract
46
what 3 animals have the intestines as an additional shock organ?
horse, pig, and cat
46
type I hypersensitivities, also called immediate hypersensitivity, are mediated by __________ attached to mast cells
immunoglobulin E (IgE)
46
t/f: the clinical signs of allergic disease depend in large part on the route by which antigens (allergens) enter the body
true
47
"IgG or IgM Mediated Cytotoxic Hypersensitivity" is another name for which type of hypersensitivity?
type II hypersensitivity
48
type II hypersensitivity occurs when antibodies and complement attach to normal cells and cause ___________ and ___________ of cells
opsonization and phagocytosis
49
what are the 3 effects of type II hypersensitivity reactions?
1. Complement/FcR mediated inflammation 2. opsonization & phagocytosis 3. abnormal physiologic responses without tissue injury (Ex: Myasthenia gravis)
49
blood antigens are controlled by _________ and __________
genes and inherited
50
RBCs express cell surface molecules, usually glycoproteins or glycolipids, that act as antigens and are called...
blood group antigens or erythrocyte antigens (EA)
51
t/f: animals may possess antibodies against foreign blood group antigens even when never previously exposed to foreign red cells
true
52
what are the 2 results of IgM binding donor RBC antigens?
agglutination & hemolysis
53
the action of an antibody when it cross-links multiple antigens producing clumps of antigens a) agglutination b) hemolysis
a) agglutination
53
antibody + complement - creates MAC and puts holes in RBC membrane causing hemoglobin to leak out a) agglutination b) hemolysis
b) hemolysis
54
severity of blood transfusion reactions ranges from mild febrile response to rapid death - depends mainly on the amount of...
incompatible blood transfused
54
a large number of lysed RBCs trigger ______________ and __________
blood clotting and DIC
55
if a reaction is suspected while giving a blood transfusion what should you do?
-transfusion must be stopped immediately -maintain urine flow with fluids and a diuretic
56
how do you prevent a blood transfusion reaction?
cross-matching
57
what is hemolytic disease of the newborn (HDN)?
-fetal RBCs leak into the bloodstream of their dams through the placenta -if they have incompatible blood antigens the dam makes antibodies to the fetal RBCs -in sensitized females, these anti-fetal RBC antibodies are concentrated into their colostrum -when a newborn suckles, colostrum antibodies are absorbed through the intestinal wall and cause rapid destruction of fetal RBCs
58
what four conditions must be met for HDN to occur?
-fetus must inherit a red cell antigen from its sire that's not present in its mother -the mother must be sensitized to this antigen -the mother's response must be boosted by transplacental hemorrhage/repeated pregnancies -a newborn animal must ingest colostrum containing high-tiered antibodies to its red cells
59
what are horses blood groups? (7)
EAA EAC EAD EAK EAP EAQ EAU
60
in mules, hemolytic disease of the newborn (HDN) in foals is seen in about _____%
8-10%
60
in thoroughbreds and Standardbreds, hemolytic disease of the newborn (HDN) is ___%
2%
61
hemolytic disease is a problem in mares that have had...
several foals
61
the most severe form of HDN results from the production of antibodies against the ___ antigen of the EAA system
Aa
62
anti-Aa and anti-Qa accounts for a total of ____% of HDN in foals
90%
63
t/f: antibodies produced by mares cross the placenta
false - do not cross the placenta
63
how do antibodies produced by mares reach the foal?
through colostrum
64
HDN in foals: earliest signs are ____________ and _____________
weakness and depression
65
HDN in foals: mucus membrane of affected foals may be pale and may eventually show ___________
jaundice
66
how does HDN in calves differ from HDN in foals?
-HDN is rare -usually see similar issue from vaccination containing RBCs from infected calves sensitizing the mother
66
how does HDN in pigs differ from HDN in foals?
-used to be associated with Hog Cholera vaccine -true HDN is also rare
67
HDN in calves is rare but has resulted from vaccination against ____________ or __________
anaplasmosis or babesiosis
68
what is Bovine Neonatal Pancytopenia?
-hemorrhagic disease of newborn beef calves -sudden onset of bleeding -anemia and leukopenia -bone marrow completely aplastic -traced back to the use of BVD vaccine
69
Bovine Neonatal Pancytopenia: studies showed that the colostrum of dams of these calves contained antibodies against the ____________ antigens of neonatal leukocytes and bone marrow stem cells
MHC I
70
HDN in pigs formerly occurred as a result of the use of ______ ________ vaccine containing pig blood
hog cholera
71
talk about type II hypersensitivity reactions to drugs
-drugs and antibodies may combine directly and activate Complement and RBCs will be destroyed -some drugs (Penicillin) may bind to RBCs and cause hemolytic anemia
71
type II hypersensitivity, also called ___________ hypersensitivity, occurs when antibodies (and complement) destroy normal cells
cytotoxic
72
the destruction of transfused red blood cells when administered to a mismatched recipient is an example of type ____ hypersensitivity
II
73
some drugs may bind to blood cells and make them targets of antibodies in a type ____ hypersensitivity reaction
II
74
type III hypersensitivity develops when antigens and antibodies combine to form __________ _________, which if deposited in large amounts in tissues, trigger severe inflammation
immune complexes
75
type III hypersensitivity: the prerequisite for the development of immune complex disease is the persistent presence of....
soluble antigen and antibody
75
type III hypersensitivity: timing of the clinical manifestation is usually ____-____ after exposure
6-8 hours
76
type III hypersensitivity: the most frequently affected sites include the...
lungs, kidneys, joints, and brain (i.e., where large capillary beds exist)
77
what cells and mediators are responsible for type III hypersensitivity?
-neutrophils: granule contents -macrophages: phagocyte -mast cells: granule contents -complement: Anaphylatoxins (C3a, C5a)
78
_____ and ______ are also called anaphylatoxins since, when injected in sufficient amounts, they can kill an animal in a manner similar to anaphylaxis by causing mast cells to release histamine granules = pro-inflammatory
C3a and C5a
78
______________ release oxidants and enzymes that lead to acute inflammation and tissue destruction in a type III hypersensitivity reaction
neutrophils
79
what are the two major classifications of a type III hypersensitivity?
localized and generalized
79
what is a localized type III hypersensitivity?
-immune complexes are deposited in tissues & the reaction is seen at the site of the antigen entry -the antigen is introduced into the tissue and preformed antibody in circulation binds to its antigen
80
what is a generalized or systemic type III hypersensitivity?
-there is excess antigen in the circulation -antibody in the circulation (IgG) binds to circulating antigen and forms immune complexes -immune complexes circulate and get deposited in blood filtration points
81
-local reaction seen in the skin after subcutaneous or intradermal injection of an antigenic substance (post-vaccination) -type III hypersensitivity -starts as red edematous swelling and eventually there is local hemorrhage and thrombosis; even necrosis possibly what is this reaction called?
Arthus Reaction
82
what are the common sites of immune complex deposition?
Large Capillary Beds: -skin -lungs -kidneys -joints -brain
82
how is mast cell activation in type III hypersensitivity different from a type I hypersensitivity?
-instead of IgE, receptors are stimulated by complement intermediates (C3a/C5a) or IgG -not fully activated, only some granules are released
82
example of type III hypersensitivity: -cause: Canine Adenovirus type 1 or vaccination with live modified virus -effect seen: diffuse clouding of the cornea & opacity with anterior uveitis -develops: 1-3 days post infection & usually resolves spontaneously
Blue Eye
83
example of type III hypersensitivity: -cause: inhaled antigens like mold from S. rectivirgula -effect seen: pneumonia, severe cough, and difficulty breathing -develops: 5-10 hours post exposure to moldy hay
Hypersensitivity Pneumonitis ("Farmer's Lung")
83
generalized type III hypersensitivity: immune complexes are deposited at sites of _________ __________
plasma filtration
84
example of type III hypersensitivity: -cause: immune complexes in the blood stream (after anti-toxin treatment for example) -effect seen: systemic inflammation, edema, lymph node enlargement, joint swelling, & generalized vasculitis
Serum Sickness
85
t/f: Penicillin can cause all four types of hypersensitivity
true
86
talk about Methimazole drug reaciton
-Methimazole inhibits thyroid hormone synthesis by interfering with iodine incorporation -sensitized patients develop antibodies to drug/hapten
87
immune complexes contain: IgG, IgM, IgA, and C3 associated with: infectious diseases deposits are in: Mesangial & Subendothelial regions a) type 1 Membrano-proliferative Glomerulonephritis (MPGN) b) type 2 Membrano-proliferative Glomerulonephritis (MPGN) c) type 3 Membrano-proliferative Glomerulonephritis (MPGN)
a) type 1 Membrano-proliferative Glomerulonephritis (MPGN)
87
immune complexes contain: C3 only (no antibodies) associated with: dense deposits deposits are in: glomerular basement membrane a) type 1 Membrano-proliferative Glomerulonephritis (MPGN) b) type 2 Membrano-proliferative Glomerulonephritis (MPGN) c) type 3 Membrano-proliferative Glomerulonephritis (MPGN)
b) type 2 Membrano-proliferative Glomerulonephritis (MPGN)
88
immune complexes contain: IgG, IgM, IgA, and C3 associated with: very small immune complexes deposits are in: in subepithelial region a) type 1 Membrano-proliferative Glomerulonephritis (MPGN) b) type 2 Membrano-proliferative Glomerulonephritis (MPGN) c) type 3 Membrano-proliferative Glomerulonephritis (MPGN)
c) type 3 Membrano-proliferative Glomerulonephritis (MPGN)
89
what is Glomerulonephritis?
-immune complexes deposit in the glomeruli -cause basement membrane thickening & stimulate glomerular cells to proliferate
90
local deposition of immune complexes in the lungs following inhalation of antigenic dusts causes ___________ _________
hypersensitivity pneumonitis
90
immune complexes formed in the bloodstream are deposited in the glomeruli of the kidney and cause...
membrane-proliferative glomerulonephritis
91
type _____ hypersensitivity is a feature of many viral disease, especially if the virus is not neutralized by antibodies and large amount of immune complexes are generated as a result
type III
92
what cell types are responsible for type IV hypersensitivity reaction?
T cells & macrophages are the main mediators
93
which hypersensitivity is also known as the delayed hypersensitivity?
type IV hypersensitivity (T-cell mediated/antibody independent hypersensitivity)
94
what are the 2 routes of a type IV hypersensitivity reaction to cell damage?
1. soluble antigen causes cytokine mediated inflammation from CD4 cells that injures nearby tissue 2. cell-associated antigen causes T-cell mediated killing (CTLs)
95
clinical presentation of a type IV hypersensitivity reaction
-induration: hard, raised lesions -erythema and vesicles: reddened skin and fluid filled vesicles
96
reactive chemical on skin triggers reaction by binding to PRRs such as TLR4 a) atopic dermatitis b) allergic contact dermatitis
b) allergic contact dermatitis
97
pathogenesis: type I hypersensitivity a) atopic dermatitis b) allergic contact dermatitis
a) atopic dermatitis
98
pathogenesis: type IV hypersensitivity a) atopic dermatitis b) allergic contact dermatitis
b) allergic contact dermatitis
99
clinical signs: hyperemia, urticaria (hives), and pruritus (itch) a) atopic dermatitis b) allergic contact dermatitis
a) atopic dermatitis
100
clinical signs: hyperemia, vesiculation, alopecia, and erythema a) atopic dermatitis b) allergic contact dermatitis
b) allergic contact dermatitis
101
distribution: face, nose, eyes, feet, perineum a) atopic dermatitis b) allergic contact dermatitis
a) atopic dermatitis
102
distribution: hairless areas, usually ventral abdomen and feet a) atopic dermatitis b) allergic contact dermatitis
b) allergic contact dermatitis
103
major allergens: foods and pollens, fleas, inhaled allergens a) atopic dermatitis b) allergic contact dermatitis
a) atopic dermatitis
104
major allergens: reactive chemicals, dyes in contact with skin a) atopic dermatitis b) allergic contact dermatitis
b) allergic contact dermatitis
105
diagnosis: intradermal testing, immediate response a) atopic dermatitis b) allergic contact dermatitis
a) atopic dermatitis
106
diagnosis: delayed response on patch testing a) atopic dermatitis b) allergic contact dermatitis
b) allergic contact dermatitis
107
pathology: mast cell and eosinophil infiltration, edema a) atopic dermatitis b) allergic contact dermatitis
a) atopic dermatitis
108
pathology: mononuclear cell infiltration, vesiculation a) atopic dermatitis b) allergic contact dermatitis
b) allergic contact dermatitis
109
treatment: steroids, antihistamines, hyposensitization a) atopic dermatitis b) allergic contact dermatitis
a) atopic dermatitis
110
treatment: steroids a) atopic dermatitis b) allergic contact dermatitis
b) allergic contact dermatitis
111
sources of contact allergens in animals
-insecticides in flea collars, sprays, and dips -wood preservatives -floor waxes -carpet dyes -some pollens -cream/ointments -leather products -paints -house plants -metals (nickel, etc.)
111
talk about Stevens-Johnson Syndrome
-T cell mediated hypersensitivity to drugs: antibiotics/NSAIDS -develop rash that blisters into vesicles/shed large areas of epidermis and develop skin ulcers -sloughing of the skin -type IV hypersensitivity
112
what are the 3 drugs that are commonly associated with Stevens-Johnson Syndrome
1. Antibiotics 2. Sulfadrugs 3. NSAIDs
113
patients affected with this syndrome develop a rash that blisters into vesicles, then they shed large areas of epidermis and develop skin ulcers on the mouth, lips, eyes, and or genitals
Stevens-Johnson Syndrome
114
tests if the patient's lymphocytes react to a given antigen a) T-Cell proliferation Assay b) measuring T-Cell mediated cytotoxicity c) measuring cytokine release d) ELISA
a) T-Cell proliferation Assay
115
tests if patients CTLs capable of killing affected cells a) T-Cell proliferation Assay b) measuring T-Cell mediated cytotoxicity c) measuring cytokine release d) ELISA
b) measuring T-Cell mediated cytotoxicity
116
used as an alternative TB test a) T-Cell proliferation Assay b) measuring T-Cell mediated cytotoxicity c) measuring cytokine release d) ELISA
c) measuring cytokine release
117
measures the frequency of cytokine producing cells; used to quantify active T cells (anti-cytokine bound to membrane in this case) a) T-Cell proliferation Assay b) measuring T-Cell mediated cytotoxicity c) measuring cytokine release d) ELISA
d) ELISA
118
some antigens, when injected into the skin, induce a slowly developing inflammatory response called delayed, or type ____ hypersensitivity
type IV
119
delayed hypersensitivity reactions are mainly mediated by _________ and ____________
T cells and macrophages
120
a good example of delayed hypersensitivity is the reaction of ______________ cattle to intradermal injection of tuberculin
tuberculosis
121
different form of type IV hypersensitivity occurs in allergic contact dermatitis. This is a slowly developing inflammatory response that occurs when reactive chemicals bind to skin cells and trigger ___________ responses
T cell
122
____ _______ assays for cell-mediated immunity generally focus on detecting secreted cytokines or measuring cell division induced by exposure to antigens
in vitro