Resolution of inflammation Flashcards by Lara Everett

stages in process of reinstating homeostasis after injury/infection

terminating adaptive immune responses
inflammation resolution
wound healing and repair

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what does terminating adaptive immune responses involve

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

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why does inflammation resolution involve

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

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what does wound healing and repair involve

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

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why is turning off T cells crucial

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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changes to T cells after responding to antigen

switch to th2 anti-inflammatory phenotype

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3 things that may occur after T cell chang to th2

anergy
exhaustion
activation-induced cell death

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anergy

cell can’t be activated even in optimal conditions

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exhaustion

temporary state of inactivity

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activation-induced cell death

excited cells die leading to transient lymphopenia

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what occurs at the same time as T cells turning off

T reg cells will be generated

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2 types of T reg

nTreg
iTreg

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nTreg

natural/thymically derived Tree
maintain tolerance all of the time

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iTreg

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

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what do both types of T reg cells express

CD4
CD25
CTLA4
FOXP3 transcription factor

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what will only nTreg cells express

CD62L

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why is the generation of iTreg cells from naive cells important

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

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main components of inflammation resolution q

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

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specific mediators of resolution

lipid mediators
proteins and peptides
gaseous mediators
purine
neuromodulators

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what do lipid mediators do in inflammation resolution

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

what do proteins and peptides do in inflammation resolution

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

what do gaseous mediators do in inflammation resolution

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

what do neuromodulators do in inflammation resolution

block pain signals from reaching brain

examples of lipid mediators in inflammation resolution

lipoxins
resolving
protecting
maresins

examples of proteins in inflammation resolution

annexin A1 galectins

examples of gaseous mediators in inflammation resolution

hydrogen sulphide and carbon monoxide

example of purine in in inflammation resolution

adenosine

what are neuromodulators released under the control of

vagus nerve

how can apoptotic neutrophils initiate transition to resolution

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

macrophage phenotypes

M1 M2 apoptotic cells

M1 macrophages

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

M2 macrophages

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

apoptotic macrophages

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

what will stimulate M1 macrophages

Th1 NK TNF alpha IFN gamma

what will M1 macrophages secrete

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

what will stimulate M2 macrophages

IL-13 and IL-4

qhat will M2 macrophages secrete

matrix metalloproteinases vascular endothelial growth factor, VEGF IL-10

what will stimulate apoptotic macrophages

efferocytosis IL-10

what will apoptotic macrophages release

IL-1 RA VEGF IL-10 TGF beta

what can dendritic cells be

anti-inflammatory or tolerogenic include tociluzimab and vitamin D

what type of cytokine is TGF beta

pleiotropic different effects under different circumstances

TGF beta predominant function

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

TGF beta with IL-6 and 23

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

TGF beta in T follicular helper cells

3 overlapping processes in wound healing

inflammation proliferation and regeneration maturation

inflammation in wound healing

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

proliferation and regeneration in wound healing

granulation tissue new vessels grow collagen deposited

maturation in wound healing

wound closed remodelled to increase tensile strength and return function