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chronic disease > Chronic Disease And Inflammation > Flashcards

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

A

Asthma

24
Q

What response is in appropriate in asthma

A

Th2 response.

25
Q

Which prr is linked to inappropriate th2 response from activated apc like dc in asthma

A

Tlr4

26
Q

What cytokines involved

A

Il4 and 6 activate the th2

27
Q

What accompanies acute inflammation from exposure of allergen in asthma

A

Chronic underlying inflammation

28
Q

What happens in sensitisation first exposure in asthma

A

Th2 will be activated , and it’s il4 production can impose igE class switching so after second exposure rapidly respond

29
Q

How do the il4 allow for class switching

A

T and b cell interaction

30
Q

What happens in mast cell degranulation

A

Release of cytokines, pg, lt and hsitamien = inflammation

31
Q

How are pg and lt inflmamtory

A

Promote vascular permeability

32
Q

Which cytokines from th2 aswell as mast cells can induce eosinophils recruitment

A

Il5 and 13

33
Q

Why is this an issue

A

Eosinophils promote further progressive inflammation eg via pg/lt

But also tissue damage = progressive disease via MBP and EPO toxicity

34
Q

How do eosinophils create a cycle of constant inflam via th2

A

Release of il4

35
Q

What is hyper acute rejection from and how does it cause inflammation

A

Pre-existing antibodies against ABO blood type = inflammation via complement

36
Q

How is acute different to chronic rejection

A

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
Q

What are some profibrogenic inflammatory pathways

A

Pdgf , fgf, tnfa, il 1

38
Q

Give examples of progressive disease form persistent infections

A

Cancers eg form hpv, immunodeficiency eg by hiv

Pain (from inflammatory neurones)

39
Q

How are tumour cells usually targeted

A

Neo ag presentation on hla 1 for cd8 and NK cell killing

40
Q

How may genes be inflicted in cancers and inflammation

A

May promote immune evasion

41
Q

Give example of how ros and rns can cause mutatfenesis (in chronic inflam)

A

Perxoynitrite which can react with dna in proliferating epi/stromal cells

42
Q

How do TAM promote metastasis and cancer progression

A

Vegf for neocascuslture production and mmp expression

= can escape via neovasculature easier

43
Q

Which cytokines produced by leukocytes in inflammation can suppress tp53 exp

A

Macrophage Migration inhibitor fsctor MIF

44
Q

Which immunosuppressive dc type are present in tumours

A

TADC

45
Q

How are they immunosuppressive

A

Cause T cell anergy as they lack co stimulators like b7 and cd40

46
Q

Give example of tumour releasing cytokines that are also immunosuppressive

A

Vegf and fasL

47
Q

What does tnf induce which is associated with cancer

A

Nfkb tf

48
Q

What antiapoptotic genes induced by nfkb and can be prooncogenic

A

Bc-xl, cox2, inos

49
Q

What conditions is constant acticatated nfkb genes like these seen

A

Chronic gastritis from h pylori

Ibd conditions

(Both prooncogenic)

50
Q

How is TNFa controversial in anti apoptosis

A

Also induces jnk pathway which is pro-apoptotic

51
Q

Downrefulation of what on tumour cells stops ctl and NK activity

A

MHC I (also TAP)

52
Q

Which immunosuppressive cytokines from tumours stop dc maturation

A

Il10 and Vegf

53
Q

Which cytokines increased to induce treg

A

Tgfb

54
Q

What do-inhibitory molecules is upreg on tumour cells

A

Pd-L1 which binds Pd-1 on T cells causing anergy

chronic disease (16 decks)

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