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Flashcards in Immunology 2 Deck (47):
1

What are defensins

V.small anti microbial peptides produced by leukcytes and epithelial cells that can insert themselves into membranes of microbes and disrupt their membrane

2

What secreted Ig activates complement by binding c1q?

IgM and IgG

3

What if tigger phagocyte binding?

IgG and IgA ( via FcgammaR and FcalphaR)

4

What Ig binds to mast cells?

IgE via FcelipsumR

5

What Ig bind NK cells

IgG

6

Describe neutralisation by antibodies

By binding to microbes or toxins secreted by microbes their activity can be blocked.

7

What is complement?

A collection of proteins found in circulation and tissue fluid

8

Can complement proteins act as activation enzymes?

Yes

9

What is the main event of complement activation?

The conversion of C3 to C3a and C3b

10

How is the classical pathway activated?

Antigen binds to IgM or IgG that then binds complement proteins c1q ( looks like bunch of tulips)

11

How many Ig must c1q bind to be activated?

2 or more IgG or one IgM

12

What proteins are associated with c1q?

C1r and c1s

13

How is c3 convert as formed in the classical pathway?

C1 r and c1s activate c4 and c2 and splits them into fragments

14

What two fragments form a complex that is a c3 convertase? (Classical)

C2a and c4b

15

How is the lectin pathway activated?

Acute phase protein called mannose binding lectin that is structurally similar to c1q

16

What is the difference between c1 q and mannose binding lectin?

Mannose binding lectin binds directly to microbial mannose residues but c1q binds to FC regions

17

What mannose binding lectin associated proteins activate c2 and c4?

Masp-1 and masp-2

18

What does c3b do to trigger the alternative pathway?

It binds to microbes and to another protein called factor B.

19

In the alternative pathway what does factor B do?

It splits into fragments and joins with another fragment called p. Forms 3bBbp which is another c3 convertase

20

What else does c3b bind to?

It binds to c3 convertAse which changes its substrate specificity to C5. C5 b is starting point of the membrane attack pathway

21

What does c5b stick to?

The lipid membrane surface of a microbe

22

What happens after c5b binds?

C6 and c7 join followed by c8 that inserts itself into the membrane followed by 12-14 copies of c9 that form a tubular structure with hollow centre - microbe punching hole that destroys microb

23

What are phagocytes?

Macrophages already present in tissue

24

What happens when a microbe binds to a PRR on a phagocyte

This triggers the phagocyte to release cytokines and lipid mediators but also triggers process of phagocytosis.

25

What is a phagosome?

Vesicle formed by the process of phagocytosis

26

What are lysosomes and what are their function in phagocytosis?

Lysosomes are vesicles of lytic enzymes found in cytoplasm. They bind to phagosome and release contents onto surface of the microbe.

27

How are reminants of a microbe removed from the cell


By exocytosis.

28

What is opsonisation?

Coating microbes in molecules of the immune system such as C-reactive protein and mannin binding lectin

29

How are parasites destroyed?

Killed extracellularly by eosinophils that release digestive enzymes from stored granules

30

What receptors do eosinophils ave?

FC and co olé net receptors. IgG receptors and IgE receptors once activated

31

True or false: mast cells kill microbes?

False. They do not kill anything. They promote inflammation

32

What is the benefit of inflammation?

Allows cells and molecules to infiltrate infected tissues

33

What FC receptor do Mast cells have?

IgE FC receptor. They are coated n a layer of IgE

34

IgE is important for the activation of what two cells?

Mast cells and eosinophils

35

What two ways can mast cells be activated?

By cross linking of antigen to two or more IgE on cell surface or by binding of c3b or c5a to complement receptor on mast cell

36

What do mast cells contain?

Granules packed with inflammatory mediators such as histamine and heparin

37

Upon activation what else do mast cells produce?

De novo production from arachidonic acid of leucotrines and prostaglandins - released more slowly

38

What do prostaglandins do?

They increase blood flow to infected area and chemotaxis (summon white blood cells)

39

6 stages of inflammation

1) vasodilation
2)leucocyte adhesion
3) vascular permeability
4) chemotaxis of leucocytes
5) immobilisation
6) activation

40

What are the two types of adhesion molecules that help to stick leucocytes to endothelial cells

Selectins and integrins

41

Explain the capture and roll stage

Interaction of leucocytes with selectin on endothelial,cells causes movement to slow down

42

Explain activation and flattening?

This is the second interaction of leucocytes with integrins which allows then to bind very strongly to the endothelial cell surface.

43

Explain extrarasation?

Movement of leucocyte across endothelial cell surface - squeezed between endothelial cells

44

After extrarasation what do they leucocytes do?

They move through the tissue in a directional fashion towards the infection (chemotaxis!)

45

How do macrophages improve chemotaxis?

By producing chemoattractants that form a concentration gradient.

46

What do the chemoattractants do to leucocytes?

Causes formation of integrins on end closest to the chemoattractants - improving connection with tissues and looses connection at other end - moves towards infection

47

What also happens as part of acute phase response (inflammatory response)

Fever
Leucocytes is
Acute phase protein release from liver