CE L3.2 Therapies continued Flashcards

1
Q

Patients with RA have high/low circulating levels of IL1β?

A

High

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2
Q

IL1β causes RA symptoms by inducing ……. and …….

A

PGs and collagenases

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3
Q

To block TNF you need high doses because ………..

A

TNF binds to trimeric receptors - you need high levels to ensure maximum blockage

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4
Q

TNF is found where in the cell?

A

membrane associated

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5
Q

Is TNF a
homotrimer
OR
heterotrimer?

A

homotrimer

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6
Q

TNF is part of ………………………… of cytokines.

Includes TNFα, TNFβm Fas-L and CD40

A

superfamily

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7
Q

Bac, viruses TNF, IL-1 and IL-2 all increase ………… but not necessarily …………………..

A

mRNA

but not necessarily protein

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8
Q

……………………… increases the stabilisation of mRNA during TNF production

A

LPS

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9
Q

TNF is synthesised as ………………………………………..

A

non-glycosylated membrane bound protein

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10
Q

What cleaves TNF from the membrane?

A

MMPs

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11
Q

Both membrane bound and soluble forms of TNF are active and mediate ………… and ………. effects

A

inflammatory and cytotoxic effects

through cell-cell contact

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12
Q

TNF receptors may be membrane bound or soluble (cleaved by ……………………….)

A

MMP

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13
Q

Two types of TNF receptors and their fucntions

A

TFNRI - apoptosis (recruits caspases) and gene transcription (TRAFs)
TNFRII - gene transcription (recruits TRAFs)

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14
Q

TNF receptors are basically a molecular switch to determine:

A

death or activation

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15
Q

How does TNF engage the receptor?

A

Homotrimerises

-3 chains polymerise to form triangle and C termini engage 3 receptors

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16
Q

When we target TNF we mainly target soluble OR membrane bound form?

A

Soluble

17
Q

Where does TNF act to cause fever?

A

hypothalamus

18
Q

Prolonged TNF exposure causes (2)

A

muscle wasting

septic shock

19
Q

What is TNF’s effect on hepatocytes

A

increased release of APP

20
Q

What is TNF’s effect on EC

A

induces expression of cytokines and adhesion molecules (from macrophages)

21
Q

ACUTE controlled release of TNF is good,

PROLONGED is bad

A

.