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Immunology > Exam 3: Hypersensitivity Type II and III > Flashcards

Exam 3: Hypersensitivity Type II and III Flashcards

1
Q

what type of immune response is type II hypersensitivity

A

humoral immune response

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2
Q

type II hypersensitivity characteristics

A

RBC antigens

blood transfusion between genetically different individuals, the red cell antigens will stimulate an antibody response in the recipient

Antibody + complement = RBC destruction

animals may have antibodies against foreign blood group antigens even without previous exposure

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3
Q

how do you know if you can perform a blood transfusion

A

absence of agglutination

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4
Q

what is the antibody that produces agglutination in blood

A

IgM

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5
Q

possible blood types

A 
A+
A-
B+
B-
AB+
AB-
O+
O-
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6
Q

is there an immune response if animal donor = animal recipient

A

no immune response

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7
Q

is there an immune response if animal donor does not equal animal recipient

A

yes immune response

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8
Q

what is the 1st stage?

A

hypotension
bradycardia
apnea

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9
Q

what is the 2nd stage

A

hypertension
cardiac arrhythmia
increased HR
increased respiratory rate

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10
Q

hemolytic disease of the newborn (HDN) neonatal isoerythrolysis

A
  1. newborn with different blood type than mother
    ex - mom is Aa- and baby is Aa+
  2. mother must be sensitized to this red cell antigen
  3. mother’s response must to be boosted to transplacental hemorrhage or repeated pregnancies
  4. newborn animal must ingest colostrum with high antibodies against its red cells

foal ingests antibodies against its RBC and will produce hemolytic disease

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11
Q

type II hypersensitivity to drugs

A

drugs + antibodies + complement –> bystander effect on RBC

drugs attached to RBC membrane + antibodies + complement on RBC

drugs that modify RBC membrane + antibodies = phagocytosis

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12
Q

type II hypersensitivity in infectious diseases

A

equine infectious anemia, anaplasmosis, trypanosomiasis, babesiosis –> severe anemia

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13
Q

why is there a yellow pigmentation with type II hypersensitivity

A

due to release of immunoglobulins

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14
Q

what do you use to treat type II hypersensitivity

A

has to be treated with a blood transfusion

make sure foal does not drink any more of the mother’s colostrum

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15
Q

what is needed to produce immune complex in type III hypersensitivity

A

antigen + antibody
complement

animal must have high amounts of antigens or high levels of antibodies to produce immune complex

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16
Q

what type of immune response is type III hypersensitivity associated with

A

humoral immune response

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17
Q

what is the main cell type in type III hypersensitivity

A

neutrophils

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18
Q

what do neutrophils do in type III hypersensitivity

A

release enzymes to promote inflammation

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19
Q

what do immune complexes lead to when they are deposited in tissues

A

chemotactic peptides

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20
Q

type III hypersensitivity - local type - where are IC formed

A

immune complexes are formed within the tissue

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21
Q

type III hypersensitivity - generalized type - where are IC formed

A

immune complexes are formed within the blood stream

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22
Q

type III hypersensitivity - generalized type - where are IC deposited

A

within the glomeruli in the kidney

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23
Q

local type III hypersensitivity important complement component

A

C5a

C5a is chemotactic for neutrophils

24
Q

local type III hypersensitivity - arthus reaction

A

high level of antibodies in bloodstream, antigen injected SQ

red edematous swelling, local hemorrhage, thrombosis, tissue destruction

6-8 hours reaction

first neutrophils, then macrophages = nitric oxide, chemokines, leukotrienes, cytokines

25
Q

local type III hypersensitivity - reversed arthus reaction

A

high levels of antigens, antibodies injected SQ

26
Q

what complement component attracts neutrophils

27
Q

pathogenesis of arthus reaction - macrophages

A

produce nitric oxides –> proteases and oxidants –> tissue destruction

produce proinflammatory cytokines (IL-1, TNF-a) –> enhanced selectin expression –> neutrophil emigration –> neutrophil accumulation –> degranulation –> proteases and oxidants –> tissue destruction

28
Q

pathogenesis of arthus reaction - neutrophils

A

phagocytosis –> neutrophil accumulation –> degranulation –> proteases and oxidants –> tissue destruction

29
Q

pathogenesis of arthus reaction - mast cells

A

degranulation –> proteases and oxidants –> tissue destruction

30
Q

pathogenesis of arthus reaction - activated complement

A

C5a –> neutrophil chemotaxis –> neutrophil accumulation –> degranulation –> proteases and oxidants –> tissue destruction

31
Q

local type III hypersensitivity - blue eye

A

canine adenovirus type-1

produced in response to vaccination when the dog has high levels of antibodies against canine adenovirus

inflammation of fungus of the eye

accumulation of immune complexes and neutrophils in cornea

after a few days goes back to normal

32
Q

local type III hypersensitivity - hypersensitivity pneumonitis

A

Saccharopolyspora rectivirgula

fungus in hay –> animals in contact with hay and get fungus

hypersensitivity produced

animals develop pneumonia due to constant contact with antigen

nasal secretions

33
Q

local type III hypersensitivity - staphylococcal hypersensitivity

A

chronic infection of skin causes chronic lesions from chronic exposure to antigen

34
Q

what happens to IC under normal circumstances

A

IC are removed by erythrocytes and macrophages

35
Q

what happens in generalized type II hypersensitivity where there is production of high amount of IC

A

IC get deposited in blood vessels where there is a physiological outflow of fluid

glomeruli in kidney
choroid plexus in brain
synovial membranes in joints

36
Q

Generalized type III hypersensitivity steps?

A
  1. IV antigen + circulating antibodies
  2. Immune complex (IC)
  3. Production of high amounts of IC leads to deposition on blood vessels with physiological outflow of fluid
37
Q

how are IC removed in primates

A

binding to complement receptors of RBC

carried to liver where they are transferred to Kupffer cells for phagocytosis

38
Q

what happens to IC in type III generalized in absence of complement components

A

significant accumulation of IC occurs in tissues

IC bind to receptors on platelets

39
Q

serum sickness

A

generalized type III

thrombosis, inflammation of kidney and joints

once IC eliminated, everything goes back to normal

40
Q

Generalized type III - high IC accumulate in arteries

A

neutrophil accumulation

leads to arteritis

41
Q

Generalized type III - high IC accumulate in kidney

A

proliferation response

leads to glomerulonephritis

42
Q

Generalized type III - high IC accumulate in synovial membranes

A

neutrophil accumulation

leads to arthritis

43
Q

two types of IC

A

soluble complexes

insoluble complexes

44
Q

what happens to soluble IC

A

get deposited in blood vessels walls

sometimes bound to red cells and are removed by mononuclear phagocytic cells in liver

45
Q

what happens to insoluble IC

A

removed by mononuclear phagocytic cells in liver

46
Q

glomerulus general function

A

where blood filtration occurs

47
Q

where are IC deposited in glomerulus

A

on either side of on within the basement membrane

48
Q

type I glomerulonephritis

A

mesangioproliferative glomerulonephritis –>

capillary endothelial proliferation, mesangial proliferation, capillary wall thickening –>

immune complexes contain IgG, IgM, IgA, C3 –>

in mesangial and subendothelial regions –>

type I glomerulonephritis

49
Q

type III glomerulonephritis

A

mesangioproliferative glomerulonephritis –>

capillary endothelial proliferation, mesangial proliferation, capillary wall thickening –>

immune complexes contain IgG, IgM, IgA, C3 –>

in subepithelial region –>

type III glomerulonephritis

50
Q

type II glomerulonephritis

A

mesangioproliferative glomerulonephritis –>

capillary endothelial proliferation, mesangial proliferation, capillary wall thickening –>

dense deposits within glomerular basement membrane, do not contain Ig, but do contain C3 –>

type II glomerulonephritis

51
Q

where are type I, II, and III, glomerulonephritis located in glomerulus

A

type I –> mesangial cells, capillary endothelial cells

type II –> basement membrane

type III –> epithelial cells

52
Q

what do IgG, IgM, IgA, and C3 do in glomerulonephritis

A

these can accumulate and produce inflammation

complement activation and attraction of neutrophils

53
Q

fibrosis

A

avoid normal filtration of blood

54
Q

large immune complexes

A

type I MPGN –>

mesangial and endothelial cell proliferation (IL-6) –>

TGF-B –>

fibrosis

55
Q

small immune complexes

A

Type III MPGN –>

epithelial cell proliferation

56
Q

glomerulonephritis - chronic diseases

A

viruses, bacterial infections, tumors

equine infectious anemia, infectious canine hepatitis, African swine fever, leishmaniasis, Lyme disease, pyometra, chronic pneumonia, bacterial endocarditis, tumors (lymphosarcoma, osteosarcomas, mastocytomas)

57
Q

infectious diseases with a significant type III hypersensitivity component and what are the major lesions

A

bacteria, viruses, parasites

Major lesions:
glomerulonephritis
arthritis
arteritis

Immunology (15 decks)

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