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Fundamental Immunology MCQ #1 > LECTURE 7 > Flashcards

LECTURE 7 Flashcards

1
Q

result of phagocyte migration?

A

IL1! leads to fever and signals BM to make more monocytes

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2
Q

2 general types of myeloid cells

A
  1. circulating
  2. tissue resident
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3
Q

describe circulating myeloid cells

A

high turnover rate, quickly mobilized

mononuclear = monocytes/DCs
polymorphonuclear = granulocytes

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4
Q

describe tissue resident myeloid cells

A

macrophages, TAMs, DCs, MDSCs

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5
Q

what can monocytes become?

A

GM-CSF –> DCs
M-CSF –> Macrophages

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6
Q

2 roles of monocytes

A
  1. patrol for pathogens (via PRRs)
  2. phagocytic/APC
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7
Q

where are monocytes?

A

IN BLOOD

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8
Q

differentiation of monocytes

A

highly plastic! many diff subtypes and can differentiate btwn them to change phenotype

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9
Q

3 types of monocytes (2 major ones)

A
  1. CD14++CD16- classical (major)
  2. CD14++CD16+ intermediate
  3. CD14+CD16++ non-classical (major)
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10
Q

describe classical monocytes

A

CD14+CD16-
- 90% of monocytes
- CD14 helps with TLR4 signaling
- cross endothelium to enter tissues
- pro-inflammatory!
- **can differentiate into macrophages/DCs

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11
Q

describe intermediate monocytes

A

CD14++CD16+
- pro-inflammatory (IL6, IL1, TNFa)
- good APC

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12
Q

describe non-classical monocytes

A

CD14+CD16++
- patrolling!
- remove damaged cells / debris from blood
- promote wound healing, resolution of inflammation
- induce complement, cell adhesion, phagocytosis

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13
Q

where are macrophages found?

A

in all tissues!! make up 10-15% of total cell numbers

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14
Q

when does the number of macrophages increase?

A

with increased inflammatory signals from neutrophils (1st cell to move into tissue)

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15
Q

4 basic functions of macrophages

A
  1. phagocytosis
  2. clear dead cells
  3. increase immune response
  4. APC
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16
Q

how do macrophages increase immune response?

A
  1. systemic inflammation
  2. pro-inflammatory cytokines
  3. activate neighbouring stromal and immune cells
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17
Q

difference btwn macrophages and DCs as APC

A

macrophages can only activate effector T cells

DCs activate naive T cells

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18
Q

describe activation of M1 macrophages

A

“classically activated” via IFNy

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19
Q

role of M1 macrophages

A

pro-inflammatory (TNFa), phagocytosis, bacterial clearance, proteolysis

20
Q

describe activation of M2 macrophages

A

“alternatively activated” via IL4

21
Q

role of M2 macrophages

A

anti-inflammatory, wound repair/tissue remodeling, chemokines, phagocytosis

22
Q

origin of macrophages

A

before birth, macrophages from yolk sac and fetal liver become tissue resident macrophages

upon infection, HSC in BM produce monocytes that seed the blood to move to site of infection

23
Q

2 ways DCs are produced

A
  1. leave BM as fully formed DC
  2. leave BM as monocyte that can become DC
24
Q

are there more macrophages or DCs?

A

macrophages

25
Q

where do immature DCs become mature DCs?

A

in periphery

26
Q

describe development of immature DCs to mature DCs

A

NF-kB stimulates
1. increased number of dendrites
2. increased MHC presentation
3. increased co-stimulatory molecules

then move to LN and activate naive T cells

27
Q

4 subsets of DCs1

A
  1. plasmacytoid
  2. DC1/CD141
  3. DC2/CD1
  4. MoDC
28
Q

describe plasmacytoid DCs

A

type I and III IFNs for viruses

29
Q

describe DC1/CD141

A
  • make IL12 and type III IFN
  • cross-presentation –> present exogenous Ag to CD8
  • intracellular pathogens and tumours
30
Q

describe DC2/CD1

A
  • make IL23
  • present exogenous Ag to CD4
  • extracellular pathogens
31
Q

describe MoDCs

A
  • derived from monocytes in circulation then go to tissue during infection
  • produce TNF, ROS
32
Q

describe origins of DC subsets

A

plasmacytoid, DC1, and DC2 leave BM as DCs

MoDC leave BM as monocytes

33
Q

describe lifespan of neutrophils

A

short-lived + terminally differentiated

without inflammatory stimulus –> apoptosis by macrophages (EFFEROCYTOSIS)

34
Q

where are neutrophils found?

A

abundant in blood but not in healthy tissue

35
Q

how do neutrophils move to infected tissue?

A

IL8!!!!

36
Q

why are neutrophils really good

A

highest phagocytic activity, responds fastest to infectious agents

37
Q

neutrophils in inflammation (10 stages)

A
  1. patrol in blood
  2. tether
  3. integrins (endothelium) and selectins (cell)
  4. cytoskeletal rearrangement for diapedesis
  5. migration
  6. phagocytosis
  7. NETs
  8. degranulation
  9. cytokines
  10. efferocytosis
38
Q

2 stages of phagocytosis by neutrophils

A
  1. PHAGOSOME –> contains primary granule, DEFENSIN which disrupts membrane

-fuses with-

  1. LYSOSOME –> contains secondary granule, CATHELICIDIN (mostly made by neutrophils, must be activated)
39
Q

role of MDSCs

A

inhibitory –> TGFB, IL10

40
Q

when are MDSCs found?

A

when there’s dysfunction –> cancer, autoimmunity, chronic infection

41
Q

2 types of MDSCs

A
  1. PMN-MDSC
  2. M-MDSC
42
Q

Describe PMN-MDSCs

A

phenotypically similar to neutrophils (derive from polymorphonuclear cells)

43
Q

describe M-MDSCs

A

phenotypically similar to monocytes (derive from monocytes)

44
Q

why do MDSCs develop?

A

neutrophils and monocytes get reprogrammed to be anti-inflammatory by TME and suppress nearby immune cells

45
Q

2 signals leading to MDSC development

A
  1. excess expansion of myeloid cells from BM
  2. cells move to TME and drive cells to become MDSCs (thru IFNy, TLR ligands, IL4, IL13, TGFB)

Fundamental Immunology MCQ #1 (6 decks)

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