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Chronic Disease And Inflammation Flashcards

1
Q

What are chronic inflammatory diseases

A

Clinica syndromes associated with immune system

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2
Q

What sort of issues can happen if inflammation not resolved

A

Fibrosis, tissue damage, cancer

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3
Q

Why is inflammation important

A

For migration, proliferation of immune cells and differentiation eg by cytokines

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4
Q

What do vaccines use to artificially increase more apc

A

Adjuvants eg alum to delay release of ag

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5
Q

What 3 signals involved in tcr activation

A

Binding to MHC

Costim eg cd28 to b7

Cytokines for differentiation (from prr activated macrophages)

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6
Q

What process of leukocyte migration do prr help

A

Rolling and adhesion of eg neutrophils or more monocytes = more apc

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7
Q

Which cell adhesion molecules are upreg. Mainly by cytokines from activated macrophages

A

Selectins on endothelium for rolling

Integrin on leukocytes conformational change

Bind cams like vcam and icam = tight binding

Then transmigration via pecam

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8
Q

What are these things mediated by

A

Inflam cytokines like tnf (a) and il1 (b)

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9
Q

Why do cytokines determine differentiation

A

Activate different master regulators eg tbet for th1

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10
Q

How are they always polarised

A

Can suppress eachother eg tbet suppresses th2 and 17

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11
Q

What does il4 from th2 do

A

Cause Ige class switching and upregulates recetor fc re on basophils and mast cells

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12
Q

What does il5 do

A

Activate eosinophils

Important in asthma chronic disewse

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13
Q

What released from th1 activates macrophages or cd8

A

Ifny for mac

Il2 for prolif and formation of CD8

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14
Q

Give some chronic infection examples

A

Hiv , ebv , hpv, hbv

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15
Q

Give some autoimmune examples

A

Ra
T1d
Ibd

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16
Q

What other diseases can be linked to inflam/immune system

A

Cvd atherosclerosis

Neuroinflammatory eg Alzheimer’s

Allergy/allergic asthma

Transplant disease

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17
Q

Ra is caused by auto ag and auto ab. What cells does this inflam environment cause proliferation of

A

Fibroblasts liking the synovium (FLS)

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18
Q

How does inflammation do this

A

Release of cytokines like tnf and il1b from activated apc

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19
Q

What do fls do normally

A

Control ecm and lubrication of cartilage

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20
Q

In inflamed joints. What do the fls do

A

Upregulste mmps which break down and Damage the tissue

Also cause immune cell infiltration via cytokine releqse

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21
Q

How do they allow prolonged survival or neutrophils

A

Gm-csf

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22
Q

How do they allow prolonged lymphocyte

A

Type 1 ifn

23
Q

Give a severe chronic form of allergy

24
Q

What response is in appropriate in asthma

A

Th2 response.

25
Which prr is linked to inappropriate th2 response from activated apc like dc in asthma
Tlr4
26
What cytokines involved
Il4 and 6 activate the th2
27
What accompanies acute inflammation from exposure of allergen in asthma
Chronic underlying inflammation
28
What happens in sensitisation first exposure in asthma
Th2 will be activated , and it’s il4 production can impose igE class switching so after second exposure rapidly respond
29
How do the il4 allow for class switching
T and b cell interaction
30
What happens in mast cell degranulation
Release of cytokines, pg, lt and hsitamien = inflammation
31
How are pg and lt inflmamtory
Promote vascular permeability
32
Which cytokines from th2 aswell as mast cells can induce eosinophils recruitment
Il5 and 13
33
Why is this an issue
Eosinophils promote further progressive inflammation eg via pg/lt But also tissue damage = progressive disease via MBP and EPO toxicity
34
How do eosinophils create a cycle of constant inflam via th2
Release of il4
35
What is hyper acute rejection from and how does it cause inflammation
Pre-existing antibodies against ABO blood type = inflammation via complement
36
How is acute different to chronic rejection
Acute is T cell response to foreign HLA causing inflammation eg via macrophage activation Chronic is further infiltration of these T cells and progressive fibrosis after inflammation
37
What are some profibrogenic inflammatory pathways
Pdgf , fgf, tnfa, il 1
38
Give examples of progressive disease form persistent infections
Cancers eg form hpv, immunodeficiency eg by hiv Pain (from inflammatory neurones)
39
How are tumour cells usually targeted
Neo ag presentation on hla 1 for cd8 and NK cell killing
40
How may genes be inflicted in cancers and inflammation
May promote immune evasion
41
Give example of how ros and rns can cause mutatfenesis (in chronic inflam)
Perxoynitrite which can react with dna in proliferating epi/stromal cells
42
How do TAM promote metastasis and cancer progression
Vegf for neocascuslture production and mmp expression = can escape via neovasculature easier
43
Which cytokines produced by leukocytes in inflammation can suppress tp53 exp
Macrophage Migration inhibitor fsctor MIF
44
Which immunosuppressive dc type are present in tumours
TADC
45
How are they immunosuppressive
Cause T cell anergy as they lack co stimulators like b7 and cd40
46
Give example of tumour releasing cytokines that are also immunosuppressive
Vegf and fasL
47
What does tnf induce which is associated with cancer
Nfkb tf
48
What antiapoptotic genes induced by nfkb and can be prooncogenic
Bc-xl, cox2, inos
49
What conditions is constant acticatated nfkb genes like these seen
Chronic gastritis from h pylori Ibd conditions (Both prooncogenic)
50
How is TNFa controversial in anti apoptosis
Also induces jnk pathway which is pro-apoptotic
51
Downrefulation of what on tumour cells stops ctl and NK activity
MHC I (also TAP)
52
Which immunosuppressive cytokines from tumours stop dc maturation
Il10 and Vegf
53
Which cytokines increased to induce treg
Tgfb
54
What do-inhibitory molecules is upreg on tumour cells
Pd-L1 which binds Pd-1 on T cells causing anergy

Chronic Disease (16 decks)

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