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OLD "MIC 661" > Quiz 8 > Flashcards

Quiz 8 Flashcards

1
Q

What are 3 inflammatory cytokines?

A

TNF-a
IL-1B
IL-6

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2
Q

What is TNF-a main function?

A

master regulator

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3
Q

What is IL-1B main function?

A

fever response

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4
Q

What is IL-6 main function?

A

produces acute phase proteins

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5
Q

What cell produces the inflammatory cytokines?

A

macrophages

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6
Q

______ is required for production of IL-1B and IL-6

A

TNF-a

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7
Q

TNF-a increases what 2 things?

A

vascular permeability
adhesion molecules

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8
Q

What inflammatory cytokine activates macrophages?

A

TNF-a

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9
Q

What are acute phase proteins?

A

proteins in the blood that increase or decrease in concentration in response to an infection

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10
Q

What is an example of an acute phase protein?

A

CRP (activates complement)

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11
Q

What are the 2 steps of activation for IL-1B?

A

priming
activation

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12
Q

What happens during the priming step of IL-1B?

A
  1. PRR recognizes PAMP/DAMPs
  2. secretion of TNF and IFN
  3. production of pro-IL-1B
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13
Q

What happens during the activation step of IL-1B?

A
  1. inflammasome activates caspace
  2. pro-IL-1B cleaved into IL-1B
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14
Q

What 2 things are special about IL-1B?

A
  1. no gene transcription is required to make it
  2. cannot leave the cell unless leakage occurs
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15
Q

What are 3 functions of neutrophils?

A
  1. phagocytosis
  2. degranulation
  3. NETosis
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16
Q

What do neutrophil nets contain?

A

LL-37 (AMP)
histones
proteases
DNA

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17
Q

Why do neutrophil nets have proteases?

A

go into nucleus and cleaves chromatin

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18
Q

What does PAD4 do?

A

de-condenses chromatin by changing charge on Arg causing histones to release DNA

19
Q

What is the synovial membrane?

A

allows nutrients and cell exchange between joints and blood

20
Q

What is the problem cell in the synovial membrane?

A

FLS

21
Q

When immune cells infiltrate the synovium, it swells and become a __________

A

pannus

22
Q

What 3 things is inside an inflamed synovium (pannsu)

A
  1. macrophages
  2. osteoclasts
  3. invasive FLS
23
Q

___________ produce MMP that destroy bone

A

Osteoclasts

24
Q

____________ produce MMP that destroy cartilidge

A

FLS

25
Q

What activates osteoclasts and FLS?

A

TNF-a
IL-1B
IL-6

26
Q

What are 3 risk factors for RA?

A
  1. HLA-DRB1
  2. smoking
  3. microbiota
27
Q

What are 3 initiation factors of RA?

A
  1. CRP circulation
  2. post-translational modification (citrullination)
  3. auto-Ab (ACPAs and RF)
28
Q

What is rheumatoid factors?

A

high affinity auto-IgG directed against Fc of other IgG resulting in IgG appearing pathogen (immune complex)

29
Q

What is a type III HSR?

A

abnormal immune response mediated by the formation of immune complexes

30
Q

How does a type III HSR turn into RA?

A

immune complexes form and travel to joints

31
Q

What is citrullination?

A

changing charge on Arg from positive to neutral making it look pathogenic

32
Q

What performs citrullination?

A

PAD4

33
Q

Where does citrullination occur?

A

neutrophils

34
Q

What activates PAD4?

A

pore forming toxins produced by bacteria

35
Q

HLA-____ individuals increase risk of developing auto-Abs

A

DRB1

36
Q

What are ACPAs?

A

anti-citrullinated protein antibodies

37
Q

How are ACPAs made?

A

bacterial toxin and MAC targets neutrophils causing increased exposure of neutrophils DNA = creation of ACPA

38
Q

How does smoking increase chances of getting RA?

A

increase cell damage = increased PAD2 = increased citrullinated protiens = more ACPA

39
Q

What is epitope spreading?

A

Ab recognizes different epitopes on the same protein causing the creation of many types of auto-Abs

40
Q

How does epitope spreading occur?

A

chronic immune activation leads to increased numbers of auto-Ab specificity (more antigens presented = more antibodies)

41
Q

How does TNF-a induce RA?

A

increases vascular permiability allow immune cells/complexes to travel the body

TNFα can induce formation of osteoclasts

42
Q

Why are anti-TNF-a good RA drug?

A

prevents immune cells/complexes from traveling because TNF-a usually increases vascular perminability

43
Q

Why is blocking PAD4 useful as a therapeutic?

A

prevents citrullinated proteins from being created (no antigen now)

44
Q

Why is it useful that anti-PAD4 drugs are oral?

A

difficult to have type III HSR because no large complex can be made

OLD "MIC 661" (19 decks)

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