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lect 15.3 Flashcards

1
Q

what is the result of type 3 hypersensitivity

A

formation of antigen antibody complexes that deposit in tissues
- systemic pathogenic effects or locatlized to kidney, skin, joints

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2
Q

what is the importance of size of ag/ab complexes formed in type 3 hypersensitivity

A
  • Large complexes rapidly removed
  • small or intermediate complexes more
    pathogenic
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3
Q

what are the ags in type3

A

foreign proteins, microbial
antigens, self antigens

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4
Q

what is important in ype 3

A

integrity of mononuclear phagocytic system

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5
Q

what is the mechanism for type 3

A

activation of complement and inflammatory responses

neutrophils involved

immune complex mediated hypersensitivity

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6
Q

where are small immune xomplexes deposited when not cleared

A

in the subepithelium

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7
Q

where are large immune xomplexes deposited when not cleared

A

in the blood vessels and kidneys

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8
Q

systemic immmune complex disease

A

ags stimulate ab production and complexes formed which are noramlly cleared from circualtion but deposit in tissues inthis disease

lead to inflammatory response

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9
Q

what is the inflammatory repsone in type 3

A
  • complement activation
  • MAC formation
  • recruitment of neutrophils
  • Platelet aggregation
  • blood clots
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10
Q

what kind of disease is serum sickness

A

systemic immune complex disease identified in pre antibiotic era

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11
Q

what is the HAMA response

A

human anti mouse antibodies

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12
Q

explain how serum sickness occurs

A
  • Patients treated for infectious diseases (tetanus,
    diptheria) with horse Ab’s;
  • Ab’s to foreign Ab produced
  • Anti-horse Ab’s bind Ab and prevent further therpeutic
    benefit
  • clinical manifestations: fever, pain, skin eruptions,
    glomerulonephritis

occurs in patients treated with monoclonal antibodies made in rodents

HAMA response

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13
Q

what does the formation of circulating immune responses lead to

A
  • autoimmune diseases (SLE, RA)
  • drug reactions (penicillin, sulfonamides)
  • infectious diseases (poststreptococcal
    glomerulonephritis, meningitis, malaria)
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14
Q

goodpastures syndrome

A

type 3 and 2 hypersensitivity

  1. Production of Abs in response to viral respiratory infections
  2. Cross-reaction with normal tissue antigen in lung and kidney (molecular mimicry)

ADCC in type 2

Ig complexes in tpye 3

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15
Q

arthurs reaction

A

type 3 hypersensitivity

involves neutrophils and C3b formation of immune complexes

localized reaction

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16
Q

steps of arthurs reaction

A

PREVIOUSLY FORMED ag ab complex with igG antibodies

complement actication, thromobiss, hemmorage, acute inflammation

swelling, redness, necrosis

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17
Q

wehen does the lozalized reaction in arthurs ocur

A

4-8 hours after exposure to antigen

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18
Q

arthurs reaction responsible for reactino to

A

enviromental toxins

if patient has precipitating igG against specific protein like mold, re exposure leads to insoluble complex formation in lung tissue and

severse respiratory distress within 6-8 hours

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19
Q

what are some pulmonary typr 3 reactions

A

pigeon breeders disease

cheese washers disease

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20
Q

what is the response time of type 1 reactions

A

15-30 min

and late phase is 4-6 hours

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21
Q

what is the response time for type 2

A

mintues to hours

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22
Q

what is the response time for type 3

A

hours

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23
Q

what is cell mediated hypersensitivity

A

delayed type hypersensitivity (DTH)

24
Q

what is delayed type hypersensitivity mediated by

A

Th1 response

25
what does delayed type hypersensitivity occur in response to
some Ags/pathogens tuberculin reaction
26
timeline for delayed type hypersensitivity
1st exposure- TH1 response - sensitization phase 2nd exposure (1-2) weeks - effector phase -macrophage recruitment reaction -effector phase -firm, red swelling
27
what are some of the DTH mediating cells that occationally participate
TH17 TH2 CD8+
28
what are the antigen presenting cells for DTH response
macrophages langerhans cells
29
what does the TH1 reponse in DTH in the effector phase secrete
cytokines- IFN Y and chemokines activates macrophages
30
what do activateed macrophages in DTH effector phase cause
inc in class 2 MHC molecules inc in TNF receptors inc in oxygen radicals inc in nitric oxide
31
what do pateints sufferingfrom aids have a reduction of
CD4+ T cells and therefore loss of DTH lead to deveopment of life threatening infctions that wouldnt be life threatening if it was intact DTH resopnse
32
Examples of Type IV DTH Responses TH 1-mediated
contact sensitivity granulomatous hypersensititvity tuberculin type hypersensitivity allograft rejection
33
Chemicals causing contact sensitivity are lipid-soluble
1. penetrate the skin 2. form hapten-carrier conjugates with various self proteins
34
what test can be used for contact sensitivity
patch test solution of the suspected Ag is spread on the skin and covered; the appearance, within 3 days, of a raised, firm, red area indicates sensitivity
35
when would we check the patch test to determine sensitivity
within 3 days
36
what chemical indueces contact sensitivity in virtually all individuals
DNCB can be used to assess patient cell mediated immunity
37
what do giant cells cause
displacement of normal tissue form nodules release high concentration of lytic enzymes destroy surrounding tissue
38
what causes granulomatous hypersensitivity
ag no cleared prolonged damaging DTH response inflammatory rxn- visible granulomatous respone activation of mcarophages which adhere to each other fuse to for mmultinucleated giant cells
39
what is the alternative of TH1 granuloma reposne
loprosy by mycopacterium loprae that infects macrophages in tuberculoid form lepromatous form
40
what is the tuberculoid form of leprosy
cell mediated granuloma formation destroy most bacteria slow disease progression better survival
41
what is the lepromatous form of leprosy
high Ab production depressed cell mediated immunity many infected macrophages extensive nerve, bone, and tissue damage
42
what is the tuberculin test used for
evidence of exposure to DTH causing organisms
43
example of tuberculin test
mantoux test intraepidermal injection of purified m tuberculosis protein
44
tuberculin test resutl
previously exposed - tuberculin like lesion at site of injection 1-2 days later 2-4 days later - full reaction positive test indicated prior exposure
45
limiation of mantoux test
doesnt differentiate between exposure to pathogen and vaccination
46
what hypersensitivity does penicillin induce
any of the 4 types
47
what antibody of lymphocyte is induced in type 1
igE
48
what antibody of lymphocyte is induced in type 2
igM and igG
49
what antibody of lymphocyte is induced in type 3
igG
50
what antibody of lymphocyte is induced in type 4
Th1 cells
51
how does obesity lead to chronic inflamation
adipose tissue secreted proinflammatory cytokines
52
what are the causes of chronic inflammation
genetics plays a role in almost all of it inectious and non infectous causes obesity
53
what does insulin normally signal
to cells that they should import glucose for the cell to prevent hyperglycemia
54
what are signalling events that link obesity and inflammation to insulin resistance
FA bind to receptors that prevent glucose transport that was signalled by insulin lead ot catiation of proinflammatory singnals and isnulin resistance * Storage of glucose as glycogen in the liver is impaired * Use of glucose by muscle, fat, B cells, brain cells, etc is impaired
55
what receptors are involved in insulin resistance
TLR IL6R TNFR
56

immunology (30 decks)

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