Immunology 2 Flashcards

1
Q

What are defensins

A

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

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2
Q

What secreted Ig activates complement by binding c1q?

A

IgM and IgG

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3
Q

What if tigger phagocyte binding?

A

IgG and IgA ( via FcgammaR and FcalphaR)

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4
Q

What Ig binds to mast cells?

A

IgE via FcelipsumR

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5
Q

What Ig bind NK cells

A

IgG

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6
Q

Describe neutralisation by antibodies

A

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

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7
Q

What is complement?

A

A collection of proteins found in circulation and tissue fluid

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8
Q

Can complement proteins act as activation enzymes?

A

Yes

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9
Q

What is the main event of complement activation?

A

The conversion of C3 to C3a and C3b

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10
Q

How is the classical pathway activated?

A

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

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11
Q

How many Ig must c1q bind to be activated?

A

2 or more IgG or one IgM

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12
Q

What proteins are associated with c1q?

A

C1r and c1s

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13
Q

How is c3 convert as formed in the classical pathway?

A

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

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14
Q

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

A

C2a and c4b

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15
Q

How is the lectin pathway activated?

A

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

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16
Q

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

A

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

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17
Q

What mannose binding lectin associated proteins activate c2 and c4?

A

Masp-1 and masp-2

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18
Q

What does c3b do to trigger the alternative pathway?

A

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

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19
Q

In the alternative pathway what does factor B do?

A

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

20
Q

What else does c3b bind to?

A

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

21
Q

What does c5b stick to?

A

The lipid membrane surface of a microbe

22
Q

What happens after c5b binds?

A

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
Q

What are phagocytes?

A

Macrophages already present in tissue

24
Q

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

A

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

25
Q

What is a phagosome?

A

Vesicle formed by the process of phagocytosis

26
Q

What are lysosomes and what are their function in phagocytosis?

A

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

27
Q

How are reminants of a microbe removed from the cell

A

By exocytosis.

28
Q

What is opsonisation?

A

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

29
Q

How are parasites destroyed?

A

Killed extracellularly by eosinophils that release digestive enzymes from stored granules

30
Q

What receptors do eosinophils ave?

A

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

31
Q

True or false: mast cells kill microbes?

A

False. They do not kill anything. They promote inflammation

32
Q

What is the benefit of inflammation?

A

Allows cells and molecules to infiltrate infected tissues

33
Q

What FC receptor do Mast cells have?

A

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

34
Q

IgE is important for the activation of what two cells?

A

Mast cells and eosinophils

35
Q

What two ways can mast cells be activated?

A

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
Q

What do mast cells contain?

A

Granules packed with inflammatory mediators such as histamine and heparin

37
Q

Upon activation what else do mast cells produce?

A

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

38
Q

What do prostaglandins do?

A

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

39
Q

6 stages of inflammation

A

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

40
Q

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

A

Selectins and integrins

41
Q

Explain the capture and roll stage

A

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

42
Q

Explain activation and flattening?

A

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

43
Q

Explain extrarasation?

A

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

44
Q

After extrarasation what do they leucocytes do?

A

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

45
Q

How do macrophages improve chemotaxis?

A

By producing chemoattractants that form a concentration gradient.

46
Q

What do the chemoattractants do to leucocytes?

A

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

47
Q

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

A

Fever
Leucocytes is
Acute phase protein release from liver