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Defence > RIIS > Flashcards

RIIS Flashcards

1
Q

Why is the adaptive immune system not apt for new pathogens?

A

→too slow

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2
Q

Compare innate and adaptive immune system

A

→Adaptive immunity – involves very specific recognition of infectious agent
→Innate immunity – no specific antigen recognition

→Innate immunity involves recognition of broadly conserved features of different classes of pathogens

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3
Q

How is pattern recognition done in innate response?

A

→PAMPs

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4
Q

What are PAMPs?

A

→Molecules present only on pathogens and not on host cells

→Essential for survival of pathogens

→Invariant structures shared by entire class of pathogens

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5
Q

What type of bacteria have PAMPs?

A

→gram negative or positive

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6
Q

Example of PAMPs in gram negative bacteria

A

→lipopolysaccharides (LPSs) outer membrane

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7
Q

Examples of gram positive bacteria cell wall components

A

→teichoic acid
→lipoteichoic acid
→peptidoglycan found in outer membrane

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8
Q

What are other PAMPs?

A

→Bacterial flagellin
→Abnormal protein glycosylation
→Abnormal nucleic acids - viruses

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9
Q

What are PRRs?

A

→Host factors that specifically recognise a particular type of PAMP

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10
Q

How are PRRs encoded?

A

→germ line encoded

→no rearrangement unlike antibodies

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11
Q

What are the 3 types of PRRs?

A

→Extracellular
→intracellular
→secreted

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12
Q

What are secreted PRRs?

A

→they act to tag circulating pathogens for elimination

→eg complements

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13
Q

What are the components of innate immunity?

A 
→The inflammatory response
→Phagocytes
Monocytes/granulocytes/neutrophils
→Complement
→Cytokines, chemokines and anti-microbial peptides (AMPs)
→Natural Killer cells
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14
Q

What is an inflammatory response?

A

→localize and eliminate injurious agents and to remove damaged tissue components

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15
Q

What are the features of inflammatory response?

A

→Enhanced permeability and extravasation
→Neutrophil recruitment
→Enhanced cell adhesion
→Enhance clotting

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16
Q

What is the inflammatory response trigger?

A

→the release of pro-inflammatory cytokines and chemokines

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17
Q

What is the difference between cytokines and chemokines?

A

→cytokines enhance inflammatory

→chemokines act to create chemical concentration gradient for neutrophils to migrate to

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18
Q

What are TLRs not involved in?

A

→phagocytosis

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19
Q

What is a distinct feature of phagocytic recognition?

A

→they use different pattern recognition receptors

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20
Q

What are neutrophils involved in?

A

→Neutrophils involved in tissue damage not involved in priming adaptive response

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21
Q

What are the three distinct roles of macrophages and dendritic cells?

A

→Phagocytosis; material is destroyed in lysosomes
→activated macrophages produce cytokines and chemokines

→Peptides from broken down pathogens can be presented through MHC and promote the development or recall of an adaptive T cell response

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22
Q

How do Phagocytes know what to eat?

A

→By detecting phosphatidylserine on exterior membrane surface (cells undergoing apoptosis)

→By detecting “atypical sugars” (e.g. mannose, fucose, b-glucan) on cell surfaces

→By Scavenger receptors

→By “passive sampling”

→By detecting complement
proteins bound to the
pathogen surface

23
Q

What are examples of atypical sugars?

A

→mannose,
→fucose,
→b-glucan

24
Q

Which virus doesn’t present phosphatidylserine?

A

→Ebola

25
Q

What is the complement system?

A

→Complement proteins act as secreted Pattern recognition receptors (PRRs)
→can be activated by a range of PAMPs, and can also be activated by “altered self”

26
Q

Which organ makes the complement system?

A

→liver

27
Q

What are the PAMP targets of the complement system?

A 
→antigens
→LPS
→abnormal phospholipids
→atypical glycosylation
→lack of host control factors
28
Q

What are the three pathways of complement system?

A

→The Classical Pathway
→The Mannose-Binding Lectin Pathway
→The Alternative Pathway

29
Q

What is the classical pathway of complements?

A

→activated when a complement protein called C1q binds either directly to a pathogen, or onto an antigen-antibody complex

30
Q

What do all the pathways have in common?

A

→produce C3 convertase

31
Q

What is the MBL/ficolins pathway?

A

→detect carbohydrates containing mannose on the surface of pathogens,
→activating a protease called MASP
→MASP is responsible for cleaving complement components
→activates cascade

32
Q

What is the alternative pathway of the complement system?

A

→activated by bacterial endotoxin

→lipopolysaccharide present on the outer membrane of gram negative bacteria

33
Q

How do Phagocytes know when they are infected and when to produce cytokines and chemokines?

A

→PAMPs are recognised by a distinct group of Pattern Recognition Receptors

34
Q

What are the PRRs on phagocytes?

A

→TLRS
→NOD-like
→RIG like

35
Q

What is the TLR ligands?

A

→LPS
→Unmethylated CpG- viral infection
→flagelin
→dsRNA or ssRNA

36
Q

What is the outcome of TLR activation?

A

→inflammation: cytokine release (TNF, IL-1, IL-12)

→enhanced killing: reactive oxygen species, NO)

37
Q

What are the ligands for NOD-like receptors?

A

→Peptidoglycan from Gram positive and negative bacteria

→Some viral DNA and RNA (indirect?)

38
Q

What is the outcome of NOD-like receptors?

A

→inflammation: cytokine release (IL-1, IL-8)

39
Q

What is the outcome of RIG-like receptors?

A

→type I interferon production

40
Q

What is the ligand for RIG-like receptors?

A

→Viral dsRNA and 5’-triphospho RNA(inproperly capped)

41
Q

What are cytokines?

A

→Act to modify the behaviour of cells in the immune response

→Most of these are called interleukins (eg. IL-1)

42
Q

What do type 3 interferons protect?

A

→epithelial surfaces

43
Q

What are interferons induced by?

A

→viral infection

44
Q

How are interferons released?

A

→Secreted hormone factors (type I and type III)

45
Q

What are anti-microbial peptides?

A

→Secreted short peptides (18-45 amino acids)

→Offer broad protection

→Some are induced by bacterial infection​

46
Q

How do anti-microbial peptides work?

A

→by disrupting cell wall leading to lysis​

47
Q

What are NK cells?

A

→Lymphocyte-like but larger with granular cytoplasm​

48
Q

What pathogens do NK cells kill?

A

→certain tumour

→virally infected cells​

49
Q

How do NK cells cause destruction?

A

→cytotoxic molecules called granzymes & perforins​

​

50
Q

How are NK cells activated?

A

→loss of self MHC molecules on target cell surfaces
→upregulation of ligands
​

51
Q

What are the two types of complement core defects?

A

→core defects (e.g. C3) linked to development of autoimmune diseases such as lupus​

→non-core defects linked to suseptibility to specific types of pathogens such as Neisseria​

52
Q

What are two macrophage deficiencies?

A

→Chronic granulomatous disease (CGD); No oxidative burst for bacterial killing​
→IRF8 mutations linked to susceptibility to TB​

53
Q

What is Aicardi-Goutieres syndrome?

A

→associated with constitutive production of inflammatory cytokines​

54
Q

What are the receptors used in innate and adaptive immunity?

A 
→innate= pattern recognition
→adaptive= Igs and TCR

Defence (31 decks)

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