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21 fall: Biochem > test 3: 62 -63 > Flashcards

test 3: 62 -63 Flashcards

1
Q

two types of immunity

A

innate and adaptive

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2
Q

innate immunity happens ___ by action by ___

A

quickly

phagocytes, dendritic cells, natural killer cells, complement cell

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3
Q

adaptive immunity happens ___ by action of ___

A

slowly

dedritic, T cells and B cells, Antibodies

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4
Q

autoimmune diseases are usually caused by problems in the ___ immune system

A

adaptive (long term T and B cells)

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5
Q

auto-inflammatory diseases are usually caused by problems in the ___ immune system

A

innate (fast acting- phagocytes)

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6
Q

FMF

A

familial mediterranean fever (type of auto- inflammatory disease caused by problem with the innate immune system.

persistent fever resistent to medications

similar to Familial Shar-Pei fever

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7
Q

___ is a response of vascularized tissues to infection or damaged tissues.

A

inflammation

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8
Q

2 types of inflammation

A

acute

chronic

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9
Q

Acute ___ goal is protective response of vascularized tissue and neutralize & eliminate agents

A

Inflammation

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10
Q

what are some things that can cause acute inflammation?

A

necrosis

bacteria/viruses

damage

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11
Q

___ (also called hypersensitivity ) are reactions in which the normally protective immune system damages the individual’s own tissues.

A

Immune reactions

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12
Q

during inflammation blood vessels will ___

A

vasodilate (get bigger)

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13
Q

What two cells are responsible for inflammation

A

neutrophils and macrophages

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14
Q

steps of inflammation

A

vasodilation

increased permeability

endothelial cell activation: important for leukocyte recruitment

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15
Q

redness in inflammation is caused by ___

A

vasodilation of blood vessels

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16
Q

vasodilation is induced by the chemical mediator ___

A

histamine

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17
Q

during vasodilation what happens?

A

histamine triggers endothelial cells to contract allowing spaces for neutrophils to leave blood flow into tissues

this allows for increased vessel diameter and fluid loss

=slower blood flow and increased viscosity

STASIS

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18
Q

STASIS

A

engorgement of small blood vessels with slowly moving red blood cells

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19
Q

what are some chemical mediators that help with endothelial cells contracting during acute inflammation response

A

histaime, bradykinin, leukotrienes

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20
Q

The vascular reactions of acute inflammation consist of changes in the ___ and the permeability of vessels, both designed to maximize the movement of plasma proteins and ___ out of the circulation and into the site of infection or injury.

A

flow of blood

leukocytes

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21
Q

___ is the loss of fluid and increased vessel diameter lead to slower blood flow, concentration of red cells in small vessels, and increased viscosity of the blood.

A

STASIS

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22
Q

As stasis develops, blood leukocytes, principally neutrophils, accumulate along the vascular endothelium due to damaged tissues expression ___.

A

adhesion molecules

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23
Q

4 steps of leukocyte getting into tissue

A

rolling

integrin activation by chemokines

stable adhesion

migration through endothelium

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24
Q

leukocytes are slowed down in the blood stream by ___ binding to ___. This activation will cause endothelial cells in the vessel wall to ___

A

integrin on leukocyte

selectin in vessel wall

contract

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25
Q

___ chemokine stimulates transmigration of leukocytes in between endothelial cells

A

PECAM1

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26
Q

leukocytes in tissue are attracted by ___ and then will ___

A

chemokines

eat (phagocyos) microbes. Eating bad things will trigger the leukocyte to produce cytokines which tigger an even bigger inflammatory response

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27
Q

macrophages that have eaten a microbe will release ___ that triggers ___

A

cytokines

inflammatory response

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28
Q

___ is the movement along a chemical gradient

A

chemotaxis

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29
Q

chemotaxis is regulated by chemical mediators such as bacterial products, ___, complement system (C5a) and arachiodonic acid metabolies

A

cytokines (chemokines, IL-8)

30
Q

cytokines (____) from macrophages enhance expression of ___ on endothelial cells

A

TNF1, IL1

selectins (will grab and slow down leukocytes in blood so that it can be pulled out into issue that needs it)

31
Q

TLR are ___

A

receptors that act as sensors that trigger inflammatory response

32
Q

3 main events of chronic inflammation

A

inflammation and tissue injury

attempts at repair

immune response

33
Q

causes of chronic inflammation

A

persistent infection

autoimmunity (attacks itself)

persistent exposure to chemicals

34
Q

what cells are involved in chronic inflammation

A

T cell

B cell

macrophage

plasma cells

35
Q

chronic inflammation will cause ___ formation in the tissues

A

fibrosis

36
Q

___ development of fibrous connective tissue in response to injury

A

fibrosis

37
Q

Tissue damage induces inflammation, and the amount of damage determines the type of inflammation (___ vs chronic)

A

acute

38
Q

•Some tissue damage requires immune responses that favor tissue repair & ___ to maintain organ function

A

fibrosis

39
Q

•Damaged epithelial cells release specific cytokines (___) that promote fibrosis

A

IL-25, IL-33, TSLP

40
Q

•Autoimmunity: when inflammatory response is inappropriately targeted to __ tissues

A

host

41
Q

•Allergies: host reacting ___ against harmless environmental substance

A

excessively

42
Q

how to stop acute inflammation

A

neutrophils are short lived (hours), work and then die. Produce stop signals

macrophages: switch in arachiodonic acid metabolite produced (from leukotrienes to lipoxins). produce anti-inflammatory cytokines. TGT-B, IL-10. Stop TNFa production

43
Q

To stop acute inflammation macrophages: switch in arachiodonic acid metabolite produced (from ___ to lipoxins). produce anti-inflammatory cytokines such as ___. Stop TNFa production

A

leukotrienes

TGT-B, IL-10

44
Q

___ is one of the first amines released during inflammation

A

histamine

45
Q

histamine is stored as ___ in mast cells

A

granules

46
Q

Histamine is released by cell ___ in response to stimuli

A

degradation

47
Q

Histamine functions through ___ types of receptors

A

4 (H1-4)

48
Q

cytokines come from ___ cells and act locally: endothelial activation and systemically: fever metabolic abnormalities, hypotension

A

macrophages, endothelial cells and mast cells

49
Q

TNFalpha

A

Tumor Necrosis Factor

cytokine which is a protein

produced by produced by fibroblasts, neutrophils, epithelial cells, smooth muscle cells

mTNF (inactive form) cleaved to active (sTNF)

regulates growth, differentiation, proliferation, apoptosis, inflammatory response

50
Q

TNFa can induce activation/inflammation or ___

A

apoptosis

51
Q

TNFR1 can lead to apoptosis in the cell by __

A

death domain

TNFa binds to TNFR1

this recuits DISC proteins TRADD,FADD and TRAF2

activates caspase-8

and leads to apoptosis

52
Q

TNFR2 leads to cell activation by ___

A

TNFa binds to TNFR2

recruits DISC protein: TRAF2

this binds to NIK (NF-KB) inducing kinase

this activates TNFa gene transcription

NK-KB global activator of inflammatory cytokines (IL6-IL8)

53
Q

how to target TNFa

A

infliximab

antibody to bind to TNFa protein and prevent it from binding to cells

54
Q

feline infectious peritonitis is caused by ___

A

feline corona virus (FCoV)

55
Q

feline infectious peritonitis

A

caused by Feline corona virus 10%

two forms: wet and dry

Risk factors: age, genetics, stress and viral dose

56
Q

Treatment for FIP

A

TNF alpha activity neutralizing antibody causes apoptosis

and

antiviral treatment GS4415524

57
Q

IL-1

A

cytokines

IL-1 family has a bunch of members: IL-1a and IL-1b are most studied

58
Q

___ acts locally (associates with plasma membrane of secreted cell).

Widespread expression, even keratinocytes & endothelial cells

A

IL-1a

59
Q

___ is secreted & circulates systemically.

Produced by monocytes & macrophages

A

IL-1B

60
Q

IL-1 can act on dendritic cells and stimulate

A

increased cytokine production, upregulation of MHC and co stimulatory molecules

61
Q

IL-1 acts on macrophages to __

A

increase cytokine production and phagocytosis

62
Q

IL-1 acts on neutrophils to ___

A

increase survival, adhesion, oxidative burst and protease release

63
Q

IL-1 receptors acts as herterodimer, you can try to prevent this with ___ and ___

A

antagonist (IL-1Ra)

decoy receptor (IL-1R2)

64
Q

Familial Mediterranean Fever

A

recurrent fever syndrome

leukocytes- induced inflammation

-caused by mis-sense mutation in CTD of MEFV gene that produces pyrin protein

65
Q

pyrin regulates ___ assembly

A

inflammasome

pyrin binds to ASC to prevent it from binding to pro-caspase 1 and causing inflammation and fever

(pyrin is protein that goes wrong in Familiar Mediterranean Fever syndrome)

66
Q

pyrin competes with ___ to bind to ASC in the inflammation pathway

A

procaspase 1

67
Q

shar-pei dogs have ___ deposits in thickened skin

A

hyaluronic acid

68
Q

hyaluronic acid found in folds of sharpei dogs can trigger ___ immune system to stimulate inflammation

A

innate

69
Q

for hyaluronic acid, ___ is the rate limiting receptor

A

HAS2

70
Q

in shar-pei, ___ receptor is over expressed in dermal fibroblasts

A

HAS2 → dog has more receptors more hyaluronic acid → inflammation response

71
Q

the paper on Familial Shar-Pei Fever looked to find gene responsible by __

A

looked for heterozygosity between shar-pei and other breeds

chromosome 13- showed duplication for the HAS2 gene

paper did not observe a significant correlation between serum HA levels and copy number of shar-pei duplication

SNP(single nucleotide polymorphisms) associated with FSF also correlated with high selective pressure (homozygosity) at the HAS2 gene

21 fall: Biochem (44 decks)

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