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Basic Immunology- Module 1 > Inflammation > Flashcards

Flashcards in Inflammation Deck (33)
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1

What is inflammation?

a complex response of vascularised tissues to infection and damage that brings cells and molecules frmo the circulation to the sites where they are needed--response of living tissue to injury

2

What cell type characterises acute inflammation?

neutrophils

3

What cell type characterises chronic inflammation?

macrophages

4

What is a granuloma?

a focal collection of inflammatory cells at sites of tissue infection especially activated macrophages (epithelioid cells)

5

What are the 4 common components of all inflammation?

inducers; sensor cells; mediators; target tissue

6

What is an inudcer
?

exogenous or endogenous signals that report tissues stress

7

What cells handle para-inflammation?

resident macrophages or mast cells

8

What is the tissue state in para-inflammation?

stressed or malfunctioning- not basal state but not damaged or infected

9

When does sterile inflammation occur?

in the absence of infection in response to cell damage or death

10

What can cause sterile inflammation?

trauma or ischaemic injuries- creation of DAMPs

11

Give examples of diseases that sterile inflammation has been implicated in?

gout; alzhemiers; atherosclerosis

12

What TLRs recognise HMGB1?

TLR2, 4 and 9

13

What receptor recognises cholesterol crystlas?

NLRP3 and CD36 (scavenger receptor)

14

What receptors recognsie beta-amyloid?

NLRP3; CD36 and RAGE

15

What receptor recognises uric acid and monosodium urate?

NLRP3

16

What is inflammaging?

upregulation of the inflammatory response that occurs with advancing age

17

Why is there upregulation of inflammation with aging?

cumulative lifetime exposure of antigenic load or non infective antigens

18

What happens to neutrophils in inflammaging?

reduced phagocytic ability of opsonised bacteria and impaired superoxide production

19

What happens to monocytes/macrophages in inflammaging?

reduced MHC-II; reduced phagocytic ability and superoxide production

20

What happens to DCs in inflammaging?

impaired ability to phagocytose apoptotic cells; impaired migration

21

Waht happens to NK cells in inflammaging?

reduced cytotoxicity

22

what happens to B cells in inflammaging?

reduced repsonsiveness to stimualtory molecules; antibody response to vaccination

23

What is seen in the overall inflammation in inflammaging?

chronic low levels ofi nflammation concurrently with symptoms of immunosenescence

24

What happens to T cells in inflammaging?

impaired expansion and differentiation; impaired T cell help to B cells; increased pro-inflammatory cytokine release; increased memory and effector cells; reduced Tregs

25

How does the body counteract increased cytokines in the serum?

HPA axis is activated- cortisol levels increase

26

Aside from the anti-inflammatory effects of cortisol, what other effects does activation of hte HPA axis cause?

protein catabolism; bone resorption; insulin resistance

27

What can the higher levels of cortisol be counteracted with?

DHEA- although this also decreases with age

28

What is autoinflammation?

self-directed inflammation, whereby local factors at sites predisposed to disease lead to activation of innate immune cells with resultatn tissues damage

29

What is teh function of collagenous scavenger receptors?

phagocytosis of bacteria and apototic cells, endocytosis of modified LDL, adhesion

30

Waht is the function of noncollagenous scavenger receptors (CD36)

phagocytosis of apoptotic cells; diacyl lipid recognition of bacteria