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MOP > Innate immunity > Flashcards

Innate immunity Flashcards

1
Q

what is innate immunity?

A

the first line of defence

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2
Q

when is the innate immune system activated?

A

breach of physical barriers that can lead to infection

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3
Q

what are the two responses?

A

first (instant)and second (hours later)

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4
Q

what are the different defences triggered by the barriers?

A
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5
Q

what is complement

A

complement is a collection of soluble and membrane-bound proteins. (aka the first line of defence

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6
Q

where is complement made?

A

liver constitutively (no stimulus required) in a zymogen form (pro-enzyme (inactive form))

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7
Q

where can complement be found

A

blood, lymph, extracellular fluids

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8
Q

how is complement activated?

A

complement is activated through a cascade of enzymatic reactions that occur due to infection

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9
Q

what is the most important complement protein and why ?

A

C3 Without it people are more prone to infections

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10
Q

describe the key complement event

A

C3 is cleaved into two parts C3a which moves to activate other cells and C3B (larger) tags bacterium for destruction

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11
Q

what are the three activation pathways?

A
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12
Q

describe the alternative pathway of complement activation

A

iC3 levels increase in the vicinity of a pathogen
A hydrolysis event takes place and causes the recruitment of protein B which then recruits protein D
protein D can cleave B into Ba and Bb
Bb binds to C3b forming thus producing C3 convertase (iC3Bb)(soluble)
causing the cleavage of C3 to C3a, which recruits more proteins to continue the cycle and Cb, which covalently binds and tags pathogens.

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13
Q

describe how complement activation is tightly regulated with the use of properdin

A

properdin is a plasma protein that maintains C3bBb by preventing cleavage thus extending the life of C3 convertase
- postive regulator

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14
Q

describe how complement activation is tightly regulated with the use of factor H&I

A
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15
Q

describe how complement activation is tightly regulated with the use of DAF and MCP (self defence)

A
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16
Q

describe phagocytosis as a first line of defence in innate immunity

A
  • Complement activation leads to deposition of C3b on the bacterial cell surface
  • CR1 on macrophage binds C3b on bacterium
  • endocytosis of the bacterium by macrophages
    -Macrophage membranes fuse, creating a phagosomethen lysosome fusesvwith phagosome forming a phagolysosome
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17
Q

explain the effect phagocytosis has as a first line of defence to bacteria

A

-complement activation opsonisation and phagocytosis keep bacterial levels low at start of infection

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18
Q

explain how complement activation can result in cell in lysis

A

C3b binds C3 convertase to (C3bBb) to make C3b2Bb
-> a C5 convertase

C5 convertase activity results in assembly of the membrane attack complex (MAC)

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19
Q

explain how protectin (CD59) tightly regulates complement activation

A

on the cells of pathogens complement components C5-C( assemble a complex that perforates the cell membrane.

on human cells CD59 binds to the C5b678 complex and prevents recruitment of c9 to form the pore

20
Q

Complement activation induces inflammatory responses

A
21
Q

define inflammation

A

Complex, multifactorial response to infection, damage, trauma

22
Q

Is inflammation synonymous with INFECTION

A

no

23
Q

how is inflammation characterised

A

Calor (Heat)
Dolor (Pain)
Rubor (Redness)
Tumor (Swelling)

24
Q

describe acute inflammation

A

A local reaction where the Movement of proteins and cells from blood to tissue

25
Q

acute inflammation usually is predominant in what WBC type

A

neutrophils

26
Q

explain the Kinetics of acute inflammation

A

between 30 minutes and one hour after some trauma or infection exudate levels increase and comes down over two or three days. 6 to 8 hours after trauma neutrophils infiltrate and then disappear because they become apoptotic so apoptosis levels increasing and they’re coming down. Apoptosis levels disappear because mononuclear cells like monocytes ( which become macrophages in the tissue) eat those apoptic cells and migrate away.

early in the time frame of inflammation molecules like histamine and compliment a as time goes on, we get soluble factors such as prostaglandins and leukotrienes. Later on, we get cytokines like TNF alpha and interleukin 8 and interleukin 6. Lastly, some repair cytokinins like TGF beta.

27
Q

what is chronic inflammation

A

Prolonged and Non-resolving inflammation that leads to loss of function that leads to further disease
e.g. Rheumatoid arthritis

28
Q

describe how Cells of innate immunity recognise pathogens

A

recognise via pattern recognistion receptors such as manose R scavener r and glucan r which are all lectins and recognise carbs on microbacteria surface (aka pathogen associated molecular patterns) which leads tomphagocytosis

29
Q

what are Toll-like receptors (TLR)

A

Family of signalling receptors
Expressed by different cell types
Recognise different pathogens
Tailor innate immune responses to WHAT and WHERE

30
Q

explain how Toll-like receptors (TLR) sense infection

A

TLR signalling switches on cytokine production
->-Informs adaptive immunity

31
Q

how do Pathogens induce cytokine release

A
32
Q

characteristics of neutrophils

A

Neutrophils- most abundant white blood cell
Huge bone marrow reserve of mature neutrophils

Products of inflammation attract neutrophils to sites of infection

Neutrophils are adapted for working without oxygen

They will die hours after entry to infected tissue- forming pus (MYELOPEROXIDASE

33
Q

how neutraphils get out of blood

A

the infection causes local endothelia to upregulate adhesion molecules which allow neutrophils to stick via a low affinity interaction so that blood flow allows neutrophils to roll down into the vessel wall. until another firm adhision can occur cells migrate through gsaps in endothelium cells into tissue where receptors detect chemokine to cells migrae up chemokine to site of infection

34
Q

what do mast cells do

A

Release of vasoactive amines e.g. histamine
Release of cytokines e.g. TNF-a
Recruits
°Ab(antibodies)
°Complement
°Fluid (exudate) (helps AntigenPresenting Cells drain into lymph)
°Cells

35
Q

where are mast cells located

A

Resident in tissues & sub mucosae

36
Q

what activates mast cells

A

C3a and C5a activate mast cells
→ anaphylatoxins

37
Q

neutrophils eating pathogens

A
38
Q

how do pathogens die by oxygen-independent mechanism

A

Lysozyme, defensins, and elastase are all found in azurophilic granules
enzymes and NADPH oxidase components are found in specific granules
This alters pH in the phagosome to activate proteases (high pH) and acid hydrolases (low pH)

39
Q

how do pathogens die by oxygen-dependent mechanism

A

This alters pH in the phagosome to activate proteases (high pH) and acid hydrolases (low pH)
This alters pH in the phagosome to activate proteases (high pH) and acid hydrolases (low pH)

40
Q

what is Chronic granulomatous disease (CGD)

A

Mutations in genes for NADPH oxidase
No respiratory burst
No pH change in phagosome
No damage to pathogens
Infections are not cleared and remain in localised nodules - granulomas

41
Q

the effects of Inflammatory cytokines on the body

A

They are pyrogens - raise temperature
Reduce bacterial & virus growth
Enhance adaptive immunity

They stimulate the production of acute phase proteins
C-reactive protein (CRP) and Mannose-binding lectin (MBL)->(2nd response of innate immunity)

42
Q

how does Acute phase proteins enhance innate immunity

A

CRP binds to bacterial and fungal cell walls
MBL binds to mannose-containing carbohydrates
Both are opsonins (enhance phagocytosis)
Synthesis increases 1000-fold in the acute phase response

43
Q
A
44
Q

Innate Defence to viruses: the interferon response

A
45
Q

characteristics of natural killer cells

A

NK cells are the killers of innate immunity
Large granular lymphocytes
NK are lymphocyte cells of innate immunity – kill and make cytokines
Activity increases 20-100 times on exposure to the interferons
NK provide an early response to virus infection – until cytotoxic T cells are ready

People with no NK cells – persistent viral infections despite normal adaptive immune responses

46
Q

NK express inhibitory and activating receptors

A

NK are partly-activated so need to be tightly controlled
Several cell surface receptors that recognise alterations in cell surface proteins
Infection, malignancy and trauma can all cause changes in the surface characteristics of cells
NK can detect these changes

47
Q

how do NK Cells work

A

NK use their receptors to distinguish healthy and sick cells

MOP (9 decks)

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