Innate Immunity Flashcards

1
Q

What is innate immunity?

A

Rapid cellular/soluble component immune response present from birth, using PAMPs/DAMPs to detect microbial structures and damage as well as missing self

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2
Q

Name the 4 types of defensive barrier

A

Anatomical
Physiological
Phagocytic
Inflammatory

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3
Q

What are the anatomical barriers?

A

Skin (mechanical)

Mucous membranes

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4
Q

What are the physiological barriers?

A

Fever
Low Stomach pH
Chemical mediators: Lysozymes, interferons, complement

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5
Q

What are phagocytes?

A

Cells that ingest material

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6
Q

What is the inflammatory barrier?

A

Local increased vascular permeability to allow cell escape to enhance immune function

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7
Q

Name the major phagocytic cell types:

All 7 of ‘em!

A
Neutrophils
Eosinophils
Basophils
Monocytes/Macrophages
Mast Cells
Dendritic cells
Natural Killer Cells
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8
Q

What are neutrophils?

A

Phagocytes with multi-lobed nuclei.

Short lived; circulate in blood then migrate to tissues

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9
Q

Which cells are first recruited to the site of damage?

A

Neutrophils

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10
Q

Which cells defend against parasitic infection?

A

Eosinophils

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11
Q

What are eosinophils?

A

Phagocytes.
Release granules to defend against parasites
Help B-cells produce IgA

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12
Q

What are basophils?

A

Granule releasing cells

They act as antigen-presenting cells for antibody mediated immunity

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13
Q

What is the difference between Monocytes and Macrophages?

A

Monocytes in blood

Macrophages in tissue

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14
Q

What are macrophages?

A

Important for phagocytosis
“Big Eaters”
Release cytokines
Present antigen fragments to T-cells

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15
Q

What are mast cells?

A

Release histamine-containing granules

Pro-inflammatory

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16
Q

What do dendritic cells do?

A

Capture antigens and present them to T-cells

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17
Q

What do Natural Killer Cells do?

A

Lyse infected cells
(no antigen-specific receptors)
Secreet Interferon-y

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18
Q

How do neutrophils enter tissues?

A

Diapedesis and Chemotaxis
Simmilar way to Lymphocytes
Selectin Binding (with rollin’)
Then Integrin activation and strong binding, immobilisation and Diapedesis

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19
Q

What proportion of leukocytes are neutrophils?

A

50-70%

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20
Q

What causes a neutrophil to enter a tissue?

A

Damage causes chemokines to be released which bind to endothelial layer.
Neutrophils recept these which actiates integrin…

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21
Q

How do Neutrophils know where to go once they enter a tissue?

A

Chemotaxis:

They follow the gradient of chemokines which gets stronger towards the site of damage/infection

22
Q

Which molecules function as opsonins?

A

Antibodies and Complement

23
Q

What is Opsoninisation?

A

Coating of microorganism with opsonins (e.g. antibodies) to facilitate phagocytosis.

24
Q

What are the 2 mechanisms Neutrophils use to kill?

A

Oxygen independent: Enzymes (hydrolytic, lysozymes etc.) and antimicrobial peptides
Oxygen dependent: Free radicals, H2O2, anything that sounds toxic (e.g. you)

25
Q

What do neutrophils need to do to fight infection?

List the 4 steps:

A

Move from circ into tissues
Bind to pathogen
Phagocytose pathogen
Kill it

26
Q

How do neutrophils trap microbes?

A

Extracellular traps: they release granule net-like materials which form extracellular fibres to trap microbes

27
Q

What do macrophages do once they’ve eaten a pathogen?

A

Release soluble cytokines to recruit further cells

28
Q

What is (NK) target cell recognition?

A

Under viral stress, cell upregulates stress-induced molecules that activate natural killer cells and downregulate inhibitory molecules so NK cells are not inhibited to kill cell

29
Q

What are NK cells useful for fighting?

A

Viral infections

Tumours

30
Q

How are NK cells regulated?

A

Have activatory and inhibitory receptors

31
Q

Name 5 types of cytokine

A
Interleukins
Interferons
Chemokines
Growth factors
Cytotoxic tumour necrosis factors
32
Q

What do interferons do?

A

Interfere with viral replication

33
Q

What do growth factors do?

A

Help stem cells differentiate and proliferate

34
Q

What do cytotoxic tumour necrosis factors do?

A

Induce programmed cell death in target cells

35
Q

How do cytokines work?

A

Producing cell makes them in granules. Exocytose

Bind to receptors on cells, effect gene regulation (up/downregulate)

36
Q

Name the 3 locational modes of cytokine activity

A

Autocrine: on self
Paracrine: on nearby cells
Endocrine: via circulation to distant cell

37
Q

How many types of interferons are there, and what produces them?

A

2.
Only immune cells produce type 2
Many cells produce type 1

38
Q

What is complement?

A

Glycoprotein enzyme that ‘complements’ the action of a specific antibody

39
Q

Where are the components of the complement system produced?

A

Mainly liver

+ Monocytes and macrophages

40
Q

What is the complement system?

A

Complex system of ~30 glycoproteins that from a triggered enzyme cascade

41
Q

What happens to the complement system when it is activated?

A

Inactive precursors are cleaved, and the cleaved sites become pro-inflammatory molecules.

42
Q

What are the names of the 3 activation pathways of complement?

A

Classical
Alternative
Lectin

43
Q

What do all 3 complement activation pathways result in?

A

Activation of C3b; final common pathway

44
Q

What is the classical pathway?

A

Antibody binds to antigen on pathogen.

Conformational change in antibody leads to complement activation

45
Q

What is the alternative pathway?

A

Direct activation of complement system by surfaces of pathogens themselves.

46
Q

What is the Lectin pathway?

A

Lectin: Carbohydrate binding protein; antibody-independent activation.
Is a pattern recognition receptor, binds to patterns only present on pathogens

47
Q

What does activation of C3b lead to?

A

Formation of Membrane Attack Complex (MAC)

48
Q

What is the membrane attack complex?

A

What lyses infected cells or pathogens.

49
Q

What are the control mechanisms of complement?

A

Short half-life

Regulatory proteins on self cells, prevent complement mediated lysis of self (eg. CD59)

50
Q

What are the functions of complement?

A

Cell lysis
Opsoninisation
Pro-inflammatory effects
Clear Immune complexes (antibody-antigen)

51
Q

What might a systematic ‘acute-phase’ response result in increased production of?

A

C-reactive protein (clinical measurement of inflam)
Mannan-binding Lectin
Complement
Fibrinogen