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Unit 3 > W1 innate immunity > Flashcards

W1 innate immunity Flashcards

1
Q

What are the different subdivisions of the immune system?

A

Innate immunity
Adaptive immunity
Mucosal immunity
Clinical immunology
Memory and vaccination

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2
Q

What is the immune system?

A

A collection of cells and chemicals that work together to protect the body from disease whilst protecting the bodies own cells.

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3
Q

What are some key locations involved in the immune system?

A

Leukocytes are produced in the bone marrow, some mature in the lymph nodes.
Immune chemicals are produced by immune or damaged cells.
Immune cells circulate in the blood, lymphatic system or located in iterstital fluid.
Spleen
Thymus
Adenoids
Tonsils
Pyers patches etc.

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4
Q

What does the immune system protect the body from?

A

Malignancy such as cancer cells and the causing toxins and pollutants.
Bacteria
Viruses
Parasites
Fungi

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5
Q

What is the key difference between innate and adaptive immunity?

A

Innate is non-specific and has an immediate response
Adaptive is specific to a pathogen and slower to act.

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6
Q

What is the difference between humoral and cellular immunity?

A

Humoral - action of proteins and chemicals, things that are dissolved in solution such as antibodies
Cellular - action of cellular mechanisms to identify and kill pathogens that use the whole cell, e.g phagocytosis.

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7
Q

What is the hierarchy of immune responses from contact with a microbe?

A

Anatomical/ physical barriers
Innate humoral factors
Innate immune cells
Adaptive immune cells and antibodies
Immune memory
(Does not always progress all the way, may be effectively managed at physical barrier or innate)

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8
Q

Often how long does it take for the adaptive immune response to be activated?

A

One day to 7 days
Presence of memory cells increases speed closer to one day, on first infection it is often closer to 7 days.

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9
Q

Where can microbes enter the body?

A

Respiratory tract
Skin
Eyes
Gastrointestinal tract
Genitourinary tract

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10
Q

What are some physical barriers to stop microbes from entering the body?

A

Hair
Wax
Membranes
Specialist epithelial cells e.g cilia
Tears - contains enzymes.
Mucus

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11
Q

What are some barrier defences of the immune system?

A

Defences in the structure and composition of mucus on the first layer of epithelial cells.
Fluid or air flow - less likely to attach
Enzymes - destroy
Low pH - unstable for microbe proteins
Defensins - antimicrobial peptides that disrupt cell membranes and virus envelopes
Normal microbiota - outcompete microbe
Tight epithelial junctions - so unable to get in between,
Goblet cells - mucus
Ciliated cells - push along
Tissue resident immune cells - phagocytosis

Freds Eagle Likes Dark Nights To Try Going Crazy.

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12
Q

Does inflammation require a pathogen?

A

No, Inflammation can occur if the damage is caused to a cell.
For example after a burn.

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13
Q

What is inflammation?
What are its key characteristics?

A

One of the bodies second line innate immunity defences.
Often localised to the site of damage, progresses through a series of stages then resolves back to normal.
Heat - calor
Pain - dolor
Swelling - tumour
Redness - rubor
Loss of function - function laesa.

Fancy dresses can turn out rubbish. (Boris Johnson picture)

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14
Q

What are interleukins?

A

A type of cytokine, produces by leukocytes to help regulate the immune response by acting as a ligand.
Denoted by IL.

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15
Q

What is meant by a cluster of differentiation?

A

A group of molecules that acts as a receptor on the surface of leukocytes.
Denoted by IL.

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16
Q

What molecule is essential to triggering the cardinal signs of inflammation?
What is its role?

A

Histamine
Is released from innate immune cells, platelets and damaged cells.
Binds to histamine receptors on capillary endothelium, causes vasodilation, increased blood flow and exudation of fluid from the blood into the tissue.

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17
Q

How might inflammation be triggered when no microbes are present?

A

Fragments of cells are released due to damage.
These fragments are things like DNA, RNA and protein, they are called DAMPs (Damage associated molecular proteins).
These bind to receptors on innate immune cells to trigger inflammation by causing cells to release inflammatory cytokines and histamine.

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18
Q

What is the difference between an extracellular and an intracellular pathogen?

A

Extracellular - live in the interstitial fluid
Intracellular - live within host cells, will be a small period of time when in the ECF as try to enter a host cell.

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19
Q

What type of immune response do extracellular pathogens require?

A

Humoural response,
Things like antibodies and complement and acute phase proteins.

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20
Q

What are acute phase proteins?
What causes their release?

A

Acute phase proteins are plasma proteins synthesised in the liver whose concentration varies by 25% of more during inflammation (increase or decrease).
Secretions of APPS is caused by cytokines.

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21
Q

What is the complement system?

A

Small proteins produced by the liver then circulate in the blood are activated (3 pathways) triggering an enzyme cascade of more than 20 proteins, to aid both adaptive and innate immunity (3 results).

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22
Q

What are the three different outcomes of the complement pathway?

A

Opsonisation/phagocytosis - C3b bound to pathogen surface attracts phagocytes.
Chemotaxis - C3b and C5a bound to pathogen surface and attract phagocytic cells down a chemical gradient and promote inflammation
Membrane attack complex - C3b causes a pathway that results in many molecules clumping together to form a pore in the pathogen membrane, so bursts and dies due to osmosis.

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23
Q

What are the three different ways that the complement pathway can be triggered?

NOTE In order from furthest point away from final outcome to closet.

A
  1. Classical pathway - antibody (often from memory cell) binds to antigen on pathogen surface, C1 binds to antigen antibody complex and is activated
  2. Lectin pathway - MBL, ficolins and MASPS bind to pathogen and cause C4 and C2 to combine, making C3
  3. Alternative pathway - C3 binds directly to the pathogen and is activated by chemical groups in structures on the pathogen’s surface, but not necessarily the antigen.
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24
Q

List the different acute phase proteins.

A

C-reactive protein
Serum Amyloid protein
Fibrinogen
Mannose binding Lectin
SP-A/SP-D

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25
Q

What is the function of serum amyloid protein?

A

Recruits and activates immune cells leading to the release of cytokines.

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26
Q

What is the function of C-reative protein?

A

Activates the classical complement pathway and phagocytosis in response to death cells and bacteria.

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27
Q

What is the function of fibrinogen?

A

Results in the formation of blood clots.

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28
Q

What is the function of mannose-binding lectin?

A

Activates the lectin complement pathway by recognising microbial sugars.

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29
Q

What is the function of SP-A and SP-D?

A

Interacts with and activates macrophages.
Interacts with antigen-presenting cells and t-lymphocytes to bridge the gap between innate and adaptive immunity.

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30
Q

What are the primary lymphoid organs?

A

The bone marrow and the thymus.

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31
Q

What is the role of dendritic cells?

A

Antigen presenting cells, travel to secondary lymphoid organs to activate naive T cells (Matured but not yet activated by antigen).

32
Q

What is the function of basophils?

A

Innate response
Histamine - causing inflammation
Heparin - causing blood thinning

33
Q

What is the function of eosinophils?

A

Tackle larger parasites such as worms.
Fight bacteria
Help manage inflammation

34
Q

What is the function of neutrophils?

A

Phagocytosis.
Contain granules
First responder, flood the area.
Kill the bacteria by respiratory burst and digestion.

35
Q

What is he function of macrophages?

A

Are resident in tissue, phagocytosis and production of cytokines to attract other immune cells

36
Q

What is the function of lymphocytes?

A

Aid adaptive immunity to fight infection by the production of antibodies.

37
Q

What is the function of mast cells?

A

Secrete histamine, cytokines, heparin and other chemicals when damaged.

38
Q

What is the function of natural killer cells?

A

Help destroy viruses, able to distinguish infected host cells from uninfected host cells.

39
Q

What is the function of an ILC or innate lymphoid cell?

A

Secrete cytokines to regular the adaptive and innate immune system.

40
Q

What is the role of PAMPS and DAMPs in inflammation?

A

PAMPS and DAMPS are recognised by PPRs receptor, such innate immune cells to release cytokines and chemokines.
Cytokines have pro-inflammatory affects on neighbouring cells.
Chemokines attract more wbc to the area down a concentration gradient.

41
Q

What is diapedesis?

A

The squeezing of wbc through gaps in the endothelial cells to enter the interstitial fluid from within the blood capillaries.
Only occurs in capillaries or veins.

42
Q

What is meant by innate white blood cells?

A

All white blood cells except from lymphocytes and plasma cells.

43
Q

What are the two main categories and the included subdivision of PRRs?

A

External - Toll like Receptors, Phagocytic Receptors.
Internal - cytoplasmic NOD and RIG like receptors, endosomal Toll LIke Recetors.

44
Q

What does PRRs stand for?

A

Pattern Recognition Receptors.

45
Q

Give an overview of phagocytic receptors?

A

Found on the surface of phagocytes, bind to a ligand on the pathogen surface to trigger phagocytosis.

46
Q

What are the different types of phagocytic receptors and what ligands do they recognise?

A

Complement Receptor CR1 - binds to C3b ligand receptor
Scavenger Receptor - binds to lipoproteins in bacterial cell wall.
Mannose Receptor - binds to mannose
Fc receptors - bind to antibody-antigen complex
C type lectin Receptor - Recognise B glycan sugar receptors on the fungal cell wall.

47
Q

What are the different types of TLR?
List in category, give name and the substrate they bind to.

A

External
-1/2/6 lipoproteins
-4 lipopolysaccharides
-5 flagellin

Internal/endosomal
-3 dsRNA
-8 ssRNA
-9 DNA and CpG.

48
Q

Explain the action of TLRs.
The mechanism

A

TLRs need to be hetero/homodimers to be active
PAMP binds to TLR.
Activates TIR domain.
Message is transmitted to in the cytoplasm
Transcription factor NFkB is activated and binds to DNA.
Intructs the cell to release proteins to trigger the next stage of the immune response.

49
Q

What is the function of NOD and RIG like cytoplasmic receptors?

A

Change genes transcription and alter cytokine release. By activating transcription factors.

50
Q

How do innate immune cells communicate with each other?

A
  1. Direct contact - cell to cell
  2. Cytokine release.
51
Q

Describe pro-inflammatory cytokines.

A

Have similar affects to histamine but are more longer lasting. vasodilation and exudation of fluid from blood into tissue.
Signal response to danger in the cell.
Include TNFa IL-6 and IL-1beta.
When not switched off can cause immune mediated inflammatory diseases.

52
Q

Describe anti-inflammatory cytokines>

A

INdicate that there is no danger,
this reverses the effect of inflammation.
Icludes TGFbeta and IL-10.

53
Q

What is the differene between phagocytosis and pincoytosis?
What do phagocytes do?

A

Phagocytes can do both.
Pincoytosis - smaller solutes and fluid
Phagocytosis - larger bacteria.

54
Q

Explain the process of phagocytosis.

A

Pathogen is recognised by PRR phagocytic receptor.
Engulfs pathogen, forming a phagosome, fuses with a lysosome to form a phagolysome.
Lysosome releases antimicrobial peptides such as lysozyme, and reactive oxygen species into the phagosome.
Kills pathogen by oxidative burst and pathogen is digested by enzymes.
Phagocyte becomes an antigen presenting cell.

55
Q

Explain hoe neutrophils come to cell the capillary during inflammation.

A

pro-inflammatory cytokines / histmaine causes inflammation, vasodilation occurs.
Histamine and other molecules active the endothelial cells, selections appear on the inside on the capillary endothelium.
Neutrophils form low affinity bonds with the selections, as low affinity can roll along the endothelial lining attracted up a chemokine gradient, constantly making and breaking bonds with selections.
When at area with the highest chemokine concentration forms a strong affinity bond with the endothelium, pushes through the gap between endothelial cells.
Will migrate through ECM.

56
Q

What happens if the pathogen is not killed by the innate immune response?

A

Nerve pain - stimulate by bradykins from damaged cells.
Adaptive immune response is activated.
Chronic inflammation.

57
Q

How do infected cells aid the immune response?

A

Produce interferons to inhibit viral replication.

58
Q

How can intracellular pathogens occur?

A

Escape the phagosome
Thrive in acidic conditions within the phagosome so are not killed.
Penetrate the cell from the outside (virus)

59
Q

What happens when there is an intracellular pathogen?

A

Intracellular PRRs, recognise the pathogen and release cytokines to activate natural killer cells.

60
Q

Explain the mechanism behind intracellular PRR activation.

A

Recognition of a pathogen from inside the endosome by an endosomal TLR.
TIR domains in the receptor are activated and transmit the signal to within the cytoplasm.
Interferon response Factors IRFs are assembled and bind to DNA acting as a transcription factor for proteins including interefrons to kill the microbe.

61
Q

What interferons are produced linked to their endosomal TLR?

A

TLR 3 - ligan was dsRNA - produces IRF3 - produces interferon 3
TLR 8 /7 - ligand was ssRNA - produces IRF7 - produces type 1 inteferons

62
Q

What are the three types of granules found in neutrophils?

A

Primary = azurophilic which contain peptides, such as elastase, protease and defensins.
Secondary = specific, such as collagenase, NADPH oxidase and heparinase.
Tertiary = Gelatinase and lysoszymes

63
Q

What is the pathway mechanism for NLR (NOD like receptors) signalling?

A

DAMPS and PAMPs are detected by the receptor.
NLR receptors aggregate to form an inflammasome.
Is activated, hence activated the cell by changes in gene expression to release proinflammatory cytokines.

64
Q

What is the pathway mechanism for RLP (RIG like receptors) receptors?

A

DAMPS and PAMPs act at the ligan binding to the receptor.
RLPs aggregate together, become activate.
Activate NKkB and IR3 transcription factors to produce proteins such as interferons.

65
Q

What are type 1 INFalpha/beta interferons?

A

Cytokines made by infected cells which increase antiviral mechanisms in near by cells.

66
Q

What are type 2 interferons INFy?

A

Released by adaptive immune cells to increase innate cell functions.

67
Q

What are type 3 interferons?

A

Function is not really known.
Are recognsied as being important in antiviral and antifungal infections.

68
Q

Explain how type 1 interferons prevent viral replication?

A

Type 1 bind to IFNAR,
Activates genes to degrade viral RNA and halt protein synthesis needed to make viral capsules.
They activate natural killer cells and recruit them to the area.
INF alpha and beta work in positive feedback loops to increase the amount of each other.

69
Q

What is the short hand for interferons?

A

INF

70
Q

How does the body sacrifice infected self cells to target a viral infections?

A

Uses natural killer cells.
Abnormal or infected cells have more activating than inhibiting ligands on their surface. Hence natural killer cell binds to an infected cell and is activated.
Natural Killer cells trigger apoptosis by releasing granules containing perforin and granzyme, and also produce INFaplha and INFgamma to activate other immune cells.

71
Q

What is the function of TNFa?

A

increase vascular permeability
gives rise to local inflammation
Hence activates local endothelial cells and innate immune cells.

72
Q

What conditions is TNFa associated with and how can they be treated?

A

arthritis (both types)
Crohn’s disease
Ulcerative Colitis

Treated by: Infliximab, Etanercept, Adalimumab

73
Q

What is the function of IL-6?

A

Early warning signal for tissue damage
Recruits and activates adaptive immune cells.
Cause acute phase proteins to be released from the liver.

74
Q

What conditions id IL-6 associated with and how can it be treated?

A

Rheumatoid arthiritis
Targeted by tocilizumab.

75
Q

What is the function of IL-1beta?

A

Activates vascular endothelium.
Causes local tissue damage.

76
Q

What conditions is IL-1beta associated with and what drugs are used to tackle this?

A

Neonatal Onset Multisystem Inflammatory disease
Treated by ankinra.

Unit 3 (18 decks)

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