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Immuno- 2nd test > bone and fat immunity > Flashcards

bone and fat immunity Flashcards

1
Q

M-CSF

A

released by Osteoblasts and promotes Osteaoclasts survival and proliferation

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2
Q

where is RANK expressed

A

Pre-osteoclasts and osteoclast

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3
Q

OPG (Osteoprotegerin)

A

mainly produced by OB (but also stromal and immune cells), it acts as a decoy receptor binding RANKL and preventing its effects on RANK

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4
Q

RANKL

A

key cytokine that directs terminal differentiation of preosteoclasts to osteoclast thereby driving bone resorption

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5
Q

determining bone loss vs increase

A

mainly the balance between RANKL-RANK-OPG. Any condition that alters this ratio will be associated with bone PATHOLOGY

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6
Q

Osteoblast secretes

A

M-CSF, OPG, RANKL

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7
Q

RANKL is induced by

A

proinflammatory cytokines: IL 1, 6, 8, and INF-a and especially IL 17

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8
Q

RANKL is inhibited by

A

anti-inflammatory cytokines like IL 4, 10 (inhibit OC)

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9
Q

Th1 response

A

INF-g and activated macrophages result in pro-clastogenic and bone resorption

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10
Q

Th17

A

potent OC activators. IL 17 both directly promotes OC differentiation and proliferation and stimulates OBs to make more RANKL

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11
Q

normal Th1/Th2 balance

A

suppresses Th17 via either IL-4 or INF-g suppressing IL-17 production- good

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12
Q

osteoblast come from

A

osteochondral precursors

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13
Q

osteoclast come from

A

monocyte precursors (retain some macrophage proteries)

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14
Q

Rheumatoid Arthritis

A

IL-23-stimulus unknown- appears in high levels in synovium of a joint
Th17 cells infiltrate the synovium
IL-17 activates neighboring OC and they proliferate
The RANK/RANKL/OPG balance is pro-bone loss and causes bony erosions and loss of joint function

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15
Q

Osteoporosis and menopause

A

Premenopausal state: estrogen promotes normal OB & OC function
Post menopausal state: OPG/RANKL balance is altered
High levels of RANKL cause net increase in OC activity
Blocking RANKL with a monoclonal antibody can lead to decreased bone loss

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16
Q

White adipose tissue (WAT)

A

Super endocrine organ and critical for homeostasis
Produces hormones, chemokines and cytokines
Regulates energy storage and expenditure, body mass and immune responses.
Composed of pre-adipocytes, adipocytes, stromal/vascular cells and macrophages

17
Q

2 types of macrophages in WAT

A

M1- pro-inflammatory

M2- anti-inflammatory

18
Q

Osteopontin

A

Produces by activated macrophages. pro-inflammatory and potent chemotactic signal for monocytes and macrophages. recruits macrophages and converts them to M1.

19
Q

Resistin

A

antagonist of adiponectin and promotes TNF-α and IL-6

20
Q

Macrophage cytokines in WAT

A

Osteopontin, Resistin, IL-1,6,8 & TNF-α

21
Q

adipocytes produce

A

adipocytokines- Leptin, Adiponectin, macrophage inhibitory cytokine, visfatin

22
Q

adipocytokines

A

act like cytokines & hormones and have broad spectrum effects

23
Q

Leptin

A

pro-inflammatory, incresases production of IL-1,6 and TNF-g

24
Q

Adiponectin

A

anti-inflammatory, suppresses TNF-a and opposes leptin

25
Q

Macrophage inhibitory cytokine

A

promotes adiponectin release and decreases inflammation

26
Q

Visfatin

A

pro-inflammatory and pro-angiogenic

27
Q

Normal (non-obese) WAT

A

Yin/yang relationship between inflammatory and anti-inflammatory adipocytokines with a net effect of slightly anti-inflammatory milieu in health

macrophage population in M2 phenotype

28
Q

Obese WAT

A

loss of balance
pro-inflammatory by recruiting large # of monocytes and macrophages into it
The portal vein carries the problem into the liver and (probably) also into atheromatous plaques.
Increasing evidence that gut microbiota may have strong influence on development of obesity

29
Q

How is fatty artery is “local obesity”

A

Cholesterol in the plaque attract M1 macrophages
Macrophages secrete CCL2 to attract monocytes and then prohibit them from exiting.
Big plaque to ruptured plaque is clinical problem of huge dimensions

30
Q

CCL2

A

chemokine found in coronary plaques, macrophages use it to attract more monocytes to the plaque

31
Q

Innate responses in the CNS

A

Innate immune responses in the brain are held in active suppression by microglia and Il-10 and TGF- β

32
Q

2 subsets of microglia in CNS

A
  1. migrate early in development and have DC and macrophage characteristics and act like M2 Macrophages (anti-inflammatory)
    They are highly branched and display little MHC
  2. Other subset is perivascular and derived from circulating monocytes- can cause problems
33
Q

Activation of the glial system by DAMPS/PAMPS causes

A

conversion the M2 to M1 and then they secrete pro-inflammatory cytokines
They upregulate MHC and change morphology

34
Q

IL-6 in the brain

A

causes delirium

Immuno- 2nd test (11 decks)

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