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Medicine Unit 5 > Resolution of inflammation > Flashcards

Resolution of inflammation Flashcards

1
Q

stages in process of reinstating homeostasis after injury/infection

A

terminating adaptive immune responses
inflammation resolution
wound healing and repair

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2
Q

what does terminating adaptive immune responses involve

A

regulatory cell function
removal of effector cells
long term maintenance of memory cells

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3
Q

why does inflammation resolution involve

A

return of tissue resident cells to an inactivated state
production of pro-resolving chemical mediators
removal of pro inflammatory factors

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4
Q

what does wound healing and repair involve

A

replacement of damaged cells
replacement of tissue matrix
may be healthy, function cellular tissue

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5
Q

why is turning off T cells crucial

A

T cells need repeated stimulation from signals 1 2 and 3 to function
if antigen or costimulation aren’t present and cytokine signal changes the T cells change phenotype or die

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6
Q

changes to T cells after responding to antigen

A

switch to th2 anti-inflammatory phenotype

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7
Q

3 things that may occur after T cell chang to th2

A

anergy
exhaustion
activation-induced cell death

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8
Q

anergy

A

cell can’t be activated even in optimal conditions

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9
Q

exhaustion

A

temporary state of inactivity

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10
Q

activation-induced cell death

A

excited cells die leading to transient lymphopenia

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11
Q

what occurs at the same time as T cells turning off

A

T reg cells will be generated

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12
Q

2 types of T reg

A

nTreg
iTreg

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13
Q

nTreg

A

natural/thymically derived Tree
maintain tolerance all of the time

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14
Q

iTreg

A

generated from naive T cells in tissues and reduce function of dendritic cells and other immune cells

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15
Q

what do both types of T reg cells express

A

CD4
CD25
CTLA4
FOXP3 transcription factor

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16
Q

what will only nTreg cells express

A

CD62L

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17
Q

why is the generation of iTreg cells from naive cells important

A

iTreg reduce activation signals by DC,sequester il-2 and release anti-inflammatory cytokines (Il-10 and TGF beta)

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18
Q

main components of inflammation resolution q

A

alternatively activated M2 macrophages
apoptotic neutrophils
cytokines: IL-10 and TGF beta

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19
Q

specific mediators of resolution

A

lipid mediators
proteins and peptides
gaseous mediators
purine
neuromodulators

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20
Q

what do lipid mediators do in inflammation resolution

A

‘stop’ neutrophil and eosinophil infiltration; stimulate non-phlogistic recruitment of monocytes; enhance macrophage phagocytosis of apoptotic neutrophils; increase the exit of phagocytes

21
Q

what do proteins and peptides do in inflammation resolution

A

inhibiting, reducing, and/or modulating the expression and activity of mediators.

22
Q

what do gaseous mediators do in inflammation resolution

A

act primarily as anti-inflammatory substances, promoting resolution of inflammatory processes.

23
Q

what do neuromodulators do in inflammation resolution

A

block pain signals from reaching brain

24
Q

examples of lipid mediators in inflammation resolution

A

lipoxins
resolving
protecting
maresins

25
Q

examples of proteins in inflammation resolution

A

annexin A1
galectins

26
Q

examples of gaseous mediators in inflammation resolution

A

hydrogen sulphide and carbon monoxide

27
Q

example of purine in in inflammation resolution

A

adenosine

28
Q

what are neuromodulators released under the control of

A

vagus nerve

29
Q

how can apoptotic neutrophils initiate transition to resolution

A

apoptotic neutrophils secrete signals which attract macrophages
macrophages recognise phosphatidylserine placed on outer cell membrane in apoptosis
phagocytosis (efferocytosis) of apoptotic neutrophils change macrophage phenotype to produce resolution associated factors
TGF beta induce recruited T cells to become T reg

30
Q

macrophage phenotypes

A

M1
M2
apoptotic cells

31
Q

M1 macrophages

A

pro-inflammatory
activated by PAMP, DAMP and inflammatory cytokines
involved in host defences against infection
produce NO for bacterial killing

32
Q

M2 macrophages

A

anti-inflammatory
wound healing
arise after exposure to th2 cytokines
promote angiogenesis
don’t produce NO
express reduced MHC2 and inhibit T cell responses

33
Q

apoptotic macrophages

A

arise after efferocytosis of apoptotic neutrophils
secrete repair mediators including growth factors
activate fibroblasts and total cells to make connective tissues
recuit T reg
increase angiogenesis

34
Q

what will stimulate M1 macrophages

A

Th1
NK
TNF alpha
IFN gamma

35
Q

what will M1 macrophages secrete

A

TNF alpha
chemokines
IL-6
IL-1 beta
IL-12

36
Q

what will stimulate M2 macrophages

A

IL-13 and IL-4

37
Q

qhat will M2 macrophages secrete

A

matrix metalloproteinases
vascular endothelial growth factor, VEGF
IL-10

38
Q

what will stimulate apoptotic macrophages

A

efferocytosis
IL-10

39
Q

what will apoptotic macrophages release

A

IL-1 RA
VEGF
IL-10
TGF beta

40
Q

what can dendritic cells be

A

anti-inflammatory or tolerogenic
include tociluzimab and vitamin D

41
Q

what type of cytokine is TGF beta

A

pleiotropic
different effects under different circumstances

42
Q

TGF beta predominant function

A

anti-inflammatory
produced in response to Th2 cytokine and is involved in promoting T reg formation along with IL-10

43
Q

TGF beta with IL-6 and 23

A

promote production of Th17 cells, inflammatory and involved in immune-mediated chronic inflammatory diseases

44
Q

TGF beta in T follicular helper cells

A
45
Q

3 overlapping processes in wound healing

A

inflammation
proliferation and regeneration
maturation

46
Q

inflammation in wound healing

A

blood vessels constrict sealing themselves off then dilate to allow immune cells and proteins in

47
Q

proliferation and regeneration in wound healing

A

granulation tissue
new vessels grow
collagen deposited

48
Q

maturation in wound healing

A

wound closed
remodelled to increase tensile strength and return function

Medicine Unit 5 (14 decks)

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