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Bloc F - Defense > Mar29 M3-Immunology Cardiovascular > Flashcards

Mar29 M3-Immunology Cardiovascular Flashcards

1
Q

important process other than lipids that contributes to ats

A

chronic infection and inflammation

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2
Q

chronic inflammation links what 3 CV conditions

A
  • ats
  • acute coronary syndromes
  • metabolic syndrome (htn, diabetes, dyslipidemia, obesity)
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3
Q

different types of inflammation

A
  • acute (injury)
  • chronic (systemic disease)
  • auto-inflammation (diff from auto-immunity) = periodic fever syndromes
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4
Q

autoinflammmation def

A
  • defects and-or abnormal activation of the INNATE immunity

- (auto-immunity involves T, B cells, Abs and loss of tolerance, NOT AUTO-INFLAMMATORY conditions)

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5
Q

important molecules in innate immunity also found on all kinds of cells

A

TLRs (a type of PRR), type 1 integral membrane glycoprotein with leucine rich EC domains (LRRs) motifs and a cytoplasmic domain homologous to IL-1R called toll or IL-1R or TIR domain

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6
Q

TLRs found on what cells

A

APCs, granulocytes, B, T, NK cells, platelets, epith cells, adipocytes, fibroblasts so role in immunity as well as NON immune role (metabolism)

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7
Q

key PRR families

A 
TLR 1,2,6 = recognize lipoproteins
TLR 4 = recognize LPS
TLR 5 = flagellin
*these are on cell surface**
(some are inside the cell and recognize nucleic acids)
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8
Q

TLR found in ats plaques

A

TLR-4 = the one that recognizes LPS

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9
Q

important IC protein downstream of TLRs when they’re activated

A

NF kappa B, essential in infection and ats

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10
Q

what NF kappa B does in cells with TLRs

A

cleaves pro-IL1b and pro-IL18 to IL-1b and IL-18, very potent inflammatory cytokines

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11
Q

other way to cleave pro-IL1b and pro-IL18 to IL-1b and IL-18 in cells with TLRs

A
  • NOD-like receptors called the inflammasome **most important one is called NALP3 (or NLPR3) **
  • macromolecular enzyme complex that cleaves pro-IL1b and pro-IL18 to IL-1b and IL-18
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12
Q

effect of IL1b in the body

A
  1. induces fever
  2. makes endothelial cells make IL-6. IL-6 leads to release of acute phase proteins by the liver
  3. CRP release by liver (through IL-6 from endoth effect)
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13
Q

CRP is marker for what other than infection and inflammation

A

-ATS and CVD

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14
Q

exogenous PAMPs associated with ats

A

CMV, H pylori and HSP60 in chlamydia pneumonia

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15
Q

endogenous PAMPs associated with ats

A
  • glucose
  • cholesterol
  • uric acid
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16
Q

(important) PRRs involvement in ats

A
  • in ats, monocytes get in intimal layer of coronary arteries
  • become lipid laden (loaded) macrophages called FOAM cells
  • cholesterol cristals get in them via scavenger Rs called CD36
  • oxidized LDL also gets in
  • NF kappa beta and inflammasome triggered (by the cristals) and prod of IL-1b and IL-18
  • these cytokines involved in plaque destabilization
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17
Q

IL-1b role in the pancreas (how does it cause diabetic pts to get worse due to chronic low grade inflammation)

A
  • beta cell receptors for FFA, LPS, LPS and glucose lead to IL-1b prod when activated
  • IL 1b producing beta cells die
  • IL 1b increases sugar as a consequence of that (bc you now have less insulin producing cells)
18
Q

structure of the NLPR3 protein (part of the inflammasome) + other prot that’s part of the inflammasome

A
  • NLPR3 = NBD (central), leucine rich repeat (LRR) (C-term), pyrin domain (N terminus)
  • when activated = conformational change releasing it from auto-inhibited state
  • (ASC prot also in inflammasome)
19
Q

substance that activates the inflammasome (to prod IL-1b) in ats

A

cholesterol crystals

20
Q

consequence of inflammasome knockout in mice (NLRP3 or ASC)

A

no production of IL-1b

21
Q

when cholesterol crystals appear in ats lesions

A

in early ats lesions

22
Q

cause of ats mediated thrombosis

A
  • growth of SM cells in intima + infiltration by macrophages and foam cells
  • MI and angina = plaque ruptures
  • no blood = infarction
  • key to prevent plaques and stabilize them*
23
Q

(EXAM) plaque activation and rupture is linked to what immune system component

A

TH1 (T helper cells 1) and their cytokines, especially IFN gamma

24
Q

(EXAM) important substance contributing to plaque stability

A

collagen (in fibrous cap of the plaque).

produced by SM cells

25
Q

(EXAM) what IFN-g from th1 does

A
  1. induces CD40L, boosting the prod of proteases that degrade collagen and weaken the fibrous cap
  2. inhibits prolif of SM, affecting collagen synthesis
  3. CD40L and CD40 interaction: tissue factor triggering the coagulation cascade and thrombus formation
26
Q

(EXAM) important cells in the ats plaque

A
  • T cell
  • foamy macrophages
  • SM migrating to upper layer. will produce collagen that stabilizes the plaque for a long time
27
Q

(EXAM) consequence of CD40-CD40L T cell-macrophage interaction

A
  • release of IFN gamma

- release of procoagulants, metalloproteinases, collagenases that destabilize the plaque

28
Q

2 antigens that are the reason why T cells migrate in the ats plaque

A
  • oxidized LDL

- B2 glycoprotein 1

29
Q

why macrophages and foam cells stay in the intima in ats

A

netrin 1, a neuronal cue molecule in the brain, also in ats plaque and keeps them there

30
Q

(important) why statins prevent CV death mainly

A
  • induce Foxp3 expression on naive CD4+ T cells to make functional FoxP3+ CD4+ T reg cells
  • T reg cells have an important role in stabilizing the ats plaque
  • (+ role in getting macrophages out of ats plaque via CCR7-dependent macrophage emigration pathway)
31
Q

other roles of statins on immune system + important one in CVS

A
  • role in getting macrophages out of plaque via CCR7-dependent macrophage emigration pathway
  • reduces LDL, higher HDL
  • interfere with MHC 2 Ag presentation
  • inhibit T cell prolif
  • impair Th1 diff
  • affect leukocyte motility
  • etc
32
Q

how statins affect plaque size

A
  • DOESN’T change

- LDL out but replaced with collagen = good because stabilizes the plaque

33
Q

T reg cells 2 sides to what they can do in ats

A
  • can help by suppressing T cells

- can lose foxp3 and transform into T follicular helper cells that promote ats

34
Q

important co-stimulatory molecules in the immune system

A

CD28 on T cell and B7 on APCs (B cells, macrophages) interaction

35
Q

immune senescence def

A
  • with age and with recurrent inflammation like with viruses, the expression of CD28 on T cells is downregulated
  • proportion of lymphocytes expressing CD28 goes down
36
Q

in what patients do you find CD4+CD28null cells

A
  • chronic inflammation pts
  • *accelerated ats is noted in pts with autoimmune diseases, post-transplant, metabolic syndrome, chronic and latent infections
37
Q

one cytokine for CD4 and CD8 cells that is important for plaque stability and that makes the difference between stable angina and unstable angina

A
  • IFN gamma**

- more IFN gamma in unstable angina

38
Q

why having more CD28- T cells contributes to ats and plaque rupture

A
  • release IFN gamma
  • macrophages receive it
  • release MMPs that destabilize the plaque
39
Q

2 diseases where CV event chances are higher

A
  • diabetes
  • rheumatoid arthritis
  • almost equal chances of CV event*
40
Q

immune related therapeutic opportunities to treat ats in the future

A
  • vaccinate for oxidized LDL
  • vaccinate for chronic latent viruses like CMV
  • block lymphocyte-macrophages interaction with novel Abs
41
Q

protein found to help measure CV risk

A

CRP (better than lipids)

42
Q

effect of canakinumab (IL-1b Ab) on CV risk and lipids

A
  • CV risk reduced by 50%
  • CRP reduced
  • LDL, HDL, TG unchanged
  • but fatal complications because much more infectious diseases*

Bloc F - Defense (57 decks)

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