Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y1 Fwong MCD Immunology (A) > 3 Innate Immunity > Flashcards

3 Innate Immunity Flashcards

1
Q

Q: Explain the functions of the important phagocytic cell- neutrophil.

A

A: 50-70% of leukocytes

Short-lived

Circulate in blood and migrate to tissues

First to be recruited to the site of tissue damage/infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Q: Explain the functions of the important phagocytic cells- (monocytes) macrophages.

A

A: Dispersed throughout tissues

Signal infection by releasing soluble mediators (cytokines)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Q: What are the characteristic features of a neutrophil?

A

A: Multi-lobed nucleus

Primary Granules - sites of the enzymes that are going to kill the phagocytosed pathogen (stain darker than secondary)

Secondary Granules - predominantly involved in replenishing primary granules and regulate the toxins that are produced during the lysis of phagocytosed pathogens

The granules fuse with the vacuole to form a phagolysosome.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Q: How does a neutrophil move into tissues?

A

A: Diapedesis (movement of a cell across the endothelial layer) and Chemotaxis

Chemokines are released from the site of infection where there is damage which bind to the local endothelial layer

  1. Rolling- Neutrophils will roll along the surface with low affinity interactions (binding to selectin).

Integrin will be in the low-affinity state.

  1. Integrin activation by chemokines - chemokine receptor on neutrophil binds to chemokine on endothelial surface and activates integrin converting it to the high-affinity state.
  2. Stable Adhesion - Integrin binds STRONGLY to the integrin ligand and the neutrophil is immobilised
  3. Cells migration into endothelium (tissue)- the cells then follow a chemokine gradient to figure out where to go - this is chemotaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Q: What makes neutrophil phagocytosis more effective?

A

A: Neutrophils need to be able to bind to the pathogen

This is much more effective after opsonisation (coating of the pathogen to make it easier for the neutrophils to recognise the pathogen).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Q: What are the 2 main types of opsonin?

A

A: bodies

Complement Proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Q: What is opsonisation?

A

A: coating of micro-organisms with proteins to facilitate phagocytosis

Opsonins act as adapter molecules which bind to the pathogen and link it to receptors present on the phagocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Q: Illustrate the role of opsonins.

A

A: Antibody binds to a receptor on the pathogen

Complement binds to the cell surface of the pathogen

The bound antibody and complement can then bind to the neutrophil and activate it.

(The neutrophil will engulf the bacterium and lyse it)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Q: What are 2 neutrophil killing mechanisms?

A

A: Oxygen-Independent: Generates a whole series of toxic metabolites - helps create optimal conditions for the enzymes to be able to kill the pathogens-

Enzymes
Lysozyme
Hydrolytic Enzymes
Antimicrobial Peptides (Defensins)

NEUTROPHIL EXTRACELLULAR TRAPS (NETs): When neutrophils become highly activated they release these nets that help trap extracellular bacteria and immobilise them. -> This helps other cells find these trapped bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Q: Compare macrophages and monocytes.

A

A: Monocytes leave the circulation and differentiate into macrophages

Macrophages > Monocytes (in terms of size)

Macrophages have lysosomes and are phagocytic and They have pattern recognition receptors (PRR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Q: How do macrophages function? What does this do?

A

A: signal infection by releasing soluble mediators (alarm cytokines)

This helps recruit other cells and activate subsequent adaptive immune responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Q: What are cytokines? (5)

A

A: Small secreted proteins

Involved in cell-to-cell communication

‘Messengers’ of the immune system

Powerful biological effects at low concentrations

Short-lived

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Q: Name the 5 cytokine types. Include description on 4.

A

A: Interleukins (IL-x) - between leukocytes

Interferons (IFN) - anti-viral effects

Chemokines - chemotaxis and movement

Growth Factors

Cytotoxic - tumour necrosis factor (TNF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Q: What are the types of interferon? Which cells produce them?

A

A: there are two types of interferon (type 1 and type 2) - only immune cells produce type 2 interferons - lots of other cells can produce type 1 interferon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Q: Describe the way a cytokine acts. 3 main ways.

A

A: Cytokines bind to a receptor on target cells leading to complex effects on gene expression.

Autocrine - the cell that secretes the cytokine expresses a receptor for it so the cytokine affects the cell that secreted it.
Paracrine - acts on nearby cells (e.g. type 1 interferon - a virus infected cell will produce type 1 interferon which moves to other cells and triggers an anti-viral state in those cells)
Endocrine - long distance - go into the circulation and travel to distant cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Q: Do cytokines generally act over short or long distances?

A

A: short

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Q: Which important cytokines are secreted by activated macrophages? (5)

A

A: IL-1: alarm cytokine, FEVER

TNF-a: alarm cytokine

IL-6: acute phase proteins, acts over long distances,

IL-8: chemotactic for neutrophils

IL-12: directs adaptive immunity, activates NK cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Q: What causes bacterial sepsis shock? What happens?

A

A: Massive release of alarm cytokines by activated macrophages causes septic shock.

Bacterial endotoxins cause massive release of TNF-a and IL-1 by activated macrophages.

Increased vascular permeability
Severe drop in blood pressure

19
Q

Q: How do dendritic cells act?

A

A: Phagocytose

Migrate once they’ve captured the antigen to the lymph nodes to activate T lymphocytes

Produce cytokines once they have been activated

20
Q

Q: Why are dendritic cells considered as part of innate immunity?

A

A: Can recognise PAMPs

21
Q

Q: Define a complement.

A

A: a system of functionally linked proteins that interact with one another to aid the body’s defences when antibodies combine with antigens

‘Complements’ the activity of a specific antibody

22
Q

Q: Describe the complement system.

A

A: Complex system of 30 glycoproteins found in quite high concentrations in the serum

Forms a triggered enzyme cascade system

A small initial response can be rapidly amplified .

once the inactive precursors are activated = active enzymes -> catalyse the cleavage of lots of molecules down the chain.

It can convert the next molecule along to become an active enzyme

23
Q

Q: Where are the components of the complement system made?

A

A: produced mainly in the liver, but also produced by monocytes and macrophages

24
Q

Q: What are components of the complement system synthesised as? Does this change?

A

A: INACTIVE PRECURSORS

When activated they become ACTIVE ENZYMES

25
Q

Q: What are the 3 pathways of complement activation?

A

A: CLASSICAL PATHWAY
Antibody binds to antigen - conformational change in the antibody leads to complement activation
if you have seen the bacteria before you will have antibodies against it - these antibodies will bind to the antigens and trigger activation of complement.

ALTERNATIVE PATHWAY
Direct activation by surfaces of pathogens themselves
direct contact with the bacterial surface

LECTIN PATHWAY
Antibody-independent activation by lectin (carbohydrate binding protein)

26
Q

Q: What is a lectin?

A

pattern recognition receptor and binds to carbohydrates that are only present on pathogens

27
Q

Q: What is the Y of complement? (The relationship between the pathways of activation)

A

A: Classical and alternative pathways converge at C3 (complement component 3)

Activation of C3 is a common final pathway which leads to the formation of MEMBRANE ATTACK COMPLEX (MAC) which is what lyses infected cells or bacteria.

MAC -> Cell Lysis

28
Q

Q: How is the complement pathway controlled?

A

A: Components have very short half lives

Complement is diluted in body fluids

There are specific regulatory proteins which help regulate the activity of complement- prevent complement mediated lysis of normal cells

29
Q

Q: What are pro-inflammatory molecules?

A

A: fragments that have been cleaved off to activate components of the complement system

30
Q

Q: Describe the function of complement.

A

A: activates an inflammatory response

lysis

opsonisation

clearance of immune complexes

31
Q

Q: Describe the activation of an inflammatory response by the complement system.

A

A: proinflammatory fragments bind to receptors (e.g. on mast cells) and can cause- mast cell degranulation -attract cells from the circulation as well

32
Q

Q: What is an immune complex?

A

A: antibody bound to soluble antigens

33
Q

Q: Why does the complement system have to clear immune complexes? How?

A

A:so they don’t cause inflammation of the blood vessels.

Red cells have a receptor for complement which binds to immune complexes and helps take them out of the circulation to be dealt with in the spleen

34
Q

Q: What are the 2 main types of mast cells?

A

A: Mucosal - lung

Connective Tissue - skin and peritoneal cavity

35
Q

Q: What is the role of mast cells? What do they recognise? What activates them? What is the net result?

A

A: Secrete HISTAMINES (involved in allergic responses)

Can recognise, phagocytose and kill pathogens

Pro-inflammatory fragments of the complement system can activate mast cells - these are anaphylatoxins

NET RESULT: Vasodilation, Increased Vascular Permeability

36
Q

Q: Summarise a typical (local acute) inflammatory response to a localised infection involving recruitment of neutrophils, and phagocytosis and killing bacteria.

Macraphages
cytokines
chemokines
complement
anaphylatoxins
leukocytes
neutrophils
A

A: You have tissue damage and a bacterial infection due to the damage

There will be macrophages in the tissue which have PRRs that can bind to PAMPs on the bacteria and perform phagocytosis.

The macrophages will become activated and secrete alarm cytokines and chemokines.

Alarm cytokines affect local vascular permeability so that circulating neutrophils and lymphocytes will be arrested and migrate into the tissue to the site of infection (directed by chemokines)

Complement will be activated either by the Alternative or Classical Pathways.

Complement activation will lead to production of pro-inflammatory fragments (anaphylatoxins)

Anaphylatoxins bind to receptors on mast cells - they will degranulate and the products of degranulation will affect vascular permeability and increased adhesion of circulating leukocytes.

Some of the products of degranulation are directly chemotactic for neutrophils

37
Q

Q: What is a systemic acute phase response? Characteristics? What induces it?

A

A: Sometimes local inflammatory response is accompanied by a systemic response

Characteristics: fever, increased leukocyte production (leukocytosis), production of acute phase proteins in the liver

Acute phase response is induced by the production of CYTOKINES which can act over a long distance

38
Q

Q: What are 4 acute phase proteins? What are they all?

A

A: Complement proteins themselves are acute phase proteins

C-reactive protein (CRP)

  • C polysaccharide of pneumococcus
  • Activates complement
  • Level may increase 1000 fold

Mannan-Binding Lectin (MBL)

  • Opsonin for monocytes
  • Activates complement

Complement

Fibrinogen
-Clotting

39
Q

Q: What are NK cells? What type of cells are they? What do they do? How are they activated? Why are they important?

A

A: natural killer cells

Large granulated lymphocytes

Cytotoxic - lyse target cells + Secrete interferon gamma

No antigen-specific receptor- They instead have activating and inhibitory receptors - a balance of these signals determines the response.
Have receptors which can bind to antibody-coated cells (ADCC = Antibody Dependent Cell-Mediated Cytotoxicity)

Important in defence against tumour cells and viral infections

40
Q

Q: What are the 2 types of target recognition of NK cells?

A

A: Missing Self Recognition

Induced Self Recognition

41
Q

Q: Describe missing self recognition.

A

A: type of target recognition of NK cells

Normal Healthy Cells - present MHC Class I - They are bound by receptors on NK cells which sends inhibitory signals (ligation of inhibitory NK receptors = inhibition of target cell killing)

If a cell becomes infected, MHC becomes down-regulated hence they go ‘missing’

This means that there is no longer an inhibitory signal for the inhibiting receptors of the NK cell to bind to

NK cells will try to kill the target cell

42
Q

Q: Describe induced cell recognition.

A

A: type of target recognition of NK cells

Cells start expressing molecules that are only induced by STRESS when infected

abnormal pattern of self proteins - stress patterns

NK Cells have activating receptors which recognise stress patterns

Once activated - the NK cells will try to kill the target cell

43
Q

Q: What may prolonged acute phase responses be accompanied by? Chacterised by?

A

A: an acute phase response, characterised by fever and increased production of components to fight infection

Y1 Fwong MCD Immunology (A) (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions