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Module 204 - Theme 1 > Innate immune defences and inflammation 2 > Flashcards

Innate immune defences and inflammation 2 Flashcards

1
Q

What are the functions of neutrophils?

A

Phagocytosis
Reactive oxygen + nitrogen species
Antimicrobial peptides
NETS -> neutrophil extracellular traps

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2
Q

What are the functions of macrophages?

A 
Phagocytosis 
Inflammatory mediators
Antigen presentation 
Reactive oxygen + nitrogen species 
Cytokines
Complement proteins
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3
Q

What are the functions of dendritic cells?

A 
Antigen presentation 
Co-stimulatory signals
Reactive oxygen species 
Interferons 
Cytokines
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4
Q

What are the functions of natural killer (NK) cells?

A 
Lysis of virally-infected cells
Interferon 
Macrophage activation 
Granzyme 
Perforin
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5
Q

How are phagocytes recruited?

A

Cytokines dilate local blood vessels.
Chemokines attract monocytes + neutrophils to infection -> cell adhesion molecules ICAM-1 + ICAM-2 are upregulated on endothelium which bind to integrins on leukocytes.
Rolling -> activation -> adhesion -> transendothelial migration.

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6
Q

What is required for phagocytosis and which cells can perform phagocytosis?

A

Neutrophils, dendritic cells, macrophages.
Opsonins -> complement components (C3b), collectins (mannose-binding lectin), antibodies.
Phagocytic receptors recognise opsonins -> complement, Fc, mannose, scavenger.

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7
Q

What are the antimicrobial mechanisms of phagocytes?

A 
Macrophage + neutrophil:
Acidification -> pH 3.5-4, bactericidal
Toxic oxygen-derived products 
Toxic NO
Antimicrobial peptides -> macrophage: cathelicidin, macrophage elastase-derived product, neutrophil: a+b defensins, cathelicin, BPI, lactoferricin
Lysozyme 
Neutrophil:
Competitors -> neutrophil: lactoferrin
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8
Q

What are Neutrophil Extracellular Traps (NETs)?

A

Netosis -> form of cell death -> nuclear chromatin released from cells -> traps microorganisms -> aids phagocytosis

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9
Q

What is the function of pattern recognition receptors (PRRs)

A

recognise pathogen-associated molecular patterns (PAMPs) -> important due to rapid replication rate.
C type lectin (CLRs), Toll-like (TLRs), NOD-like (NLRs), Rig-I like (RLRs), cytosolic DNA sensors (CDS).

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10
Q

What are PAMPs and DAMPs?

A

PAMPs -> peptidoglycan, lipopolysaccharide, DNA,
RNA.
Damage Associated Molecular Patterns -> molecules released from necrotic cells.

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11
Q

Which cells express C-type Lectin Receptors and what are their functions?

A

Most cell type thatphagocytose glycoproteins + microbes for antigen presentation to T lymphocytes.
Bind to carbohydrates in calcium-dependent manner.
Type I -> assist with antigen uptake by phagocytes
Type II -> fungal recognition
Soluble -> e.g. MBL binds carbohydrates on pathogen surfaces.

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12
Q

What are the two members of the toll receptor family for invertebrates and what are their functions?

A

dToll + 18-wheeler -> for development + immunity to fungal + bacterial infections

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13
Q

What is the structure of toll-like receptors?

A

Extracellular: LRR domain –> site of pathogen binding
Cytosolic side: TIR-domain
Form functional hetero/homodimers -> binding each TLR to same lipopeptide induces dimerisation -> brings cytoplasmic TIR-domain to close proximity.

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14
Q

Outline the cellular location of TLRs and their PAMPs

A 
Cell surface:
TLR-2 + TLR-6 -> diacyl lipopeptides 
TLR-2 + TLR-1 -> triacyl lipopeptides 
TLR-5 -> flagellin 
TLR-4 -> lipopolysaccharide 
Endosome:
TLR-3/10 -> dsRNA
TLR-7 -> ssRNA
TLR-8 -> ssRNA
TLR-9 -> CpG DNA
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15
Q

What is the function of TLR signalling?

A

Induces genes that function in host defence.
Pro-inflammatory + anti-inflammatory cytokines
Chemokines
MHC + co-stimulatory molecules
Antimicrobial peptides + complement components

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16
Q

What are the consequences of having the TLR adaptor protein Myd88?

A

Recurrent pyogenic bacterial infections, normal resistance to other microbes.
Improved with age possibly due to compensatory effect of adaptive immunity or other innate immune mechanisms.

17
Q

What are the consequences of TLR-3 deficiency?

A

Herpes simplex encephalitis -> inflammation of brain due toinfection with HSV-1 -> dsDNA, produces dsRNA during viral replication.
Defects in other signalling molecules in TLR3 signalling pathway -> HSE.

18
Q

Over-activation of TLRs are associated with which conditions?

A 
Infection:
HIV -> TLR-8
Sepsis, TB -> TLR-2,4
Inflammation:
SLE -> TLR-7,8,9
Alzheimer's, atherosclerosis -> TLR-2,4
19
Q

What are the TLR-agonists and antagonists that can treat potential conditions?

A 
Agonist:
Infection -> genital warts -> TLR-7 
Cancer -> melanoma -> TLR-7 ligand
Allergy –> ragweed pollen -> TLR-9
Antagonist:
Autoimmunity -> TLR-7,8,9
Sepsis -> TLR-4
20
Q

What are NLRs and what are the two major groups?

A

Cytoplasmic pattern recognition molecules.

NLRCs + NLRPs (‘C’ -> ‘caspase recruitment domain, ‘P’ -> pyrin domain).

21
Q

What are two examples of NLRCs and what are their functions?

A

Their leucine rich domain can bind to peptidoglycan:
NOD1 binds iE-DAP -> mainly Gm-ve bacteria.
NOD2 binds muramyl dipeptide -> Gm+ve + Gm-ve bacteria.

22
Q

What are the mutations of NOD2?

A

Gain of function -> early onset sarcoidosis -> granulomas develop in organs.
Loss of function -> susceptibility to Crohn’s disease.

23
Q

How are NLRPs activated?

A

Cellular stress, K+ efflux, ATP, ROS, lysosomal damage. e.g. crystals -> uric acid crystals (gout), amyloid beta (Alzheimer’s), islet amyloid polypeptide (T2DM).
Inflammasome has ASC + caspase 1 filaments, essential for IL-1 + IL-18 secretion.

24
Q

What does inflammasome activation lead to?

A

Cleavage of pro-IL-1 + pro-IL-18 to allow secretion

25
Q

What is an example of a gain of function mutation in NMRP3 and what is it treated by?

A

Cryopyrin-Associated Periodic Syndromes (CAPS):
mutations in exon 3 of NLRP3 gene -> over production of IL-1.
Anakinra (IL-1RA)

26
Q

What are the RLRs and what are their functions?

A

RIG-I + MDA5 -> sense cytoplasmic RNA, signal to induce pro-inflammatory cytokines + IFN.
RIG-I -> binds to ssRNA containing 5’-triphosphate,
recognises hep C (HCV), influenza.
MDA5 -> recognises dsRNA, detects picornavirus,
mutations (rare) -> IFN related diseases.

27
Q

What is a cytosolic DNA sensor and what is its mutation?

A

cGAS recognises viral dsDNA -> binds, converts ATP + GTP into cyclic G AMP.
STING-SAVI -> auto-inflammatory disease caused by gain-of-function mutations in STING gene ->abnormal inflammationthroughout body, especially skin, blood vessels, lungs.

28
Q

What is the function of acute phase proteins and what are they mainly produced by?

A

Liver, induced by TNF, IL-6 + IL-1 during infection + inflammation.
Activate complement -> induce opsonisation/phagocytosis.
Raised erythrocyte sedimentation rate (ESR) + CRP -> characteristic of acute phase response + used clinically to detect inflammation.

Module 204 - Theme 1 (14 decks)

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