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311 - Molecular Immunology > 2 - Innate Immunity - Angyal > Flashcards

2 - Innate Immunity - Angyal Flashcards

1
Q

At what life stages does immunity play an important role and why?

A

Major form of immunity in young children. Period between loss of maternal Abs and formation of own. Adaptive response takes around 6days to develop therefore innate critical to controlling infection.

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2
Q

What are the response times for innate/adaptive responses?

A

innate - immediately/first few hours

adaptive - around 6 days after pathogen encounter

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3
Q

Draw a diagram to illustrate the phases in response to infection (include eg pre-formed, broadly specific effectors etc).

A

q3. word

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4
Q

Name the 4 areas most likely for infection to occur

A

UG (urogenital) tract, GI tract, skin, respiratory tract

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5
Q

Name the physical barriers to infection

A

skin, tight epithelial junctions, cilia (movie the mucus)

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6
Q

Name the chemical barriers to infection

A

low pH (gut), lysozyme, antimicrobial peptides (defensins), fatty acids

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7
Q

How does the presence of commensal organisms in for eg the gut prevent the colonisation by pathogens?

A

commensals produce antimicrobials and compete w/ other species for space/nutrients etc therefore preventing pathogenic growth. can also educate and stimulate the immune system.

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8
Q

What kinds of changes can lead to commensals becoming pathogenic? Give examples of commensals that can become pathogenic.

A

changes in host immunity or changes in microbial ecosystem (eg in gut)
eg Clostridium, Lactobacillus, Bifidobacterium

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9
Q

______ ______ help prevent infection whereas secreted ____, _____ and the presence of _____ make an unfavourable environment for pathogens.

A

Mechanical barriers

chemicals, antimicrobials, commensals

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10
Q

Describe the physical barriers of keratinised skin and mucous membranes & their special features to fend off infection

A

Keratinised skin;

  • keratin and sebum made by keratinocytes. contain fatty acids, defensins.
  • shedding of skin so when infection Is etablished it is shed
  • commensals

Mucous membranes;

  • largest interface w/ environment
  • mucus and cilia (respiratory tract)
  • low pH (gut and vagina)
  • secreted enzymes eg lysozyme (tears and saliva)
  • shedding of epithelia
  • commensals
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11
Q

Draw diagrams highlighting the cell walls of G+ve and G-ve species.

A

311 -2 Word

q11.

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12
Q

What are the 2 potent activators of PRRs that are components of the cell wall (one from G+ve and one from G-ve)?

A

G+ve = lipoteichoic acid
G-ve = LPS
both endotoxins

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13
Q

What does lysozyme do and what type of bacteria is it effective against?

A

lysozyme cleaves bond w/in peptidoglycan (between MurNAc/GluNAc)

most effective in G+ve because of their large proportion of peptidgoglycan cell wall

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14
Q

Give 3 types of antimicrobial peptides and BRIEFLY describe them.

A

ALL synthesised as inactive precursors and need to be activated.

  • cathelicidins - induced in response to infection in epithelial cells and keratinocytes
  • defensins - described in next question
  • histatins - His rich, found in oral cavity
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15
Q

Describe defensins, their mode of action and name the 3 subfamily types

A

Defensins - amphipathic molecules. +vely charged and insert into -velycharged membranes. introduce pores/holes into the membrane and we get loss of osmosis regulation etc. 3 subfamilies = alpha, beta, theta (all have activity against different types of pathogens)

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16
Q

How are components of the complement system activated?

A

usually requires pairing of proenzymes, cleave each other to form an active enzymes. all components usually inert but become activated following presence of pathogen or Ab bound to pathogen

17
Q

Where are complement proteins normally made and what is the most abundant component?

A

liver

C3

18
Q

Name the enzyme that catalyses this reaction;
C3 -> C3b + C3a.
What is the bigger component?

A

C3 convertase

C3b = bigger

19
Q

What is a main feature of C3b that is exposed and how does this enable it to do its job?

A

following cleavage of C3, reactive thioester exposed, allows bonds to bacterial protein/carbohydrate to be made & bind to surface. C3b molecules that are not bound are rapidly inactivated in the fluid phase.

20
Q

Why is C3b rapidly degraded in the fluid phase?

A

because if it is not bound to anything, can be harmful to the body’s own cells

21
Q

Name the 3 pathways of complement activation that all generate a C3 convertase

A

classical, lectin, alternative

22
Q

Name the 2 structures that are associated w/ the lectin pathway and can trigger the complement cascade. state how they differ from each other

A

MBL - mannose binding lectin

Ficolins - fibrinogen binding domain instead of lectin domain/mannose binding domain

23
Q

Draw the structure of MBL and state how it is assembled.

A

Assembled into trimers that can then form bundles when associate w/ other sets of trimers.
word q3

24
Q

MBL monomers have low ___ to carbohydrates on microbial surfaces but MBL trimers associated in bundles have high ____ for carbohydrates on surfaces, such as ___ and ____

A

affinity
avidity
mannose, GluNAc

25
Q

Describe the steps of the complement cascade initiated by MBL.

A

When MBL activated (binding @ surfaces), MASP 1 activated. cleaves and activates MASP2 which cleaves C4/C2 domains -> C4bC2a = C3 convertase. complement cascade. C3 > C3b + C3a

26
Q

Draw the structure of the C1 complex and name the components.

A

C1q - sensor
C1r/s = Ser proteases
word q4.

27
Q

What structures of the C1 complex are similar to MASP domains and how are they thought to have evolved?

A

C1r/s structures. evolve through duplication of the same precursor gene

28
Q

Describe the activation of the complement cascade through C1 complex

A

C1q interacts w/ pathogen surfaces OR Abs (mainly IgM bound @ pathogen surface). which activates C1r. cleaves and activates C1s. cleaves C4/2 -> C4bC2a

29
Q

Describe how C1q binding to Abs (eg IgM) can cause > efficient phagocytosis by macrophages.

A

IgM binds @ pathogen surfaces. Binding of C1q triggers the complement cascade. Production of C3b/C4b components. Reactive thioester group means that it can bind Abs on microbial surfaces as well as cover the bacterial surfaces. . Phagocytosis by macrophages = most efficent when Abs bound to pathogen and its complement receptor are activated. (Link to adaptive immune response)

30
Q

Describe the 2 processes that generate > C3b of the alternative pathway

A

C3(H20)Bb - C3 undergoes spontaneous hydrolysis (just randomly moving around in plasma) > C3H20. binds factor B. cleaved by factor D. C3(H20)Bb = C3 convertase therefore > C3b produced following cleavage.

C3b deposited by classical/lectin pathway C3 convertase. bound by Factor B. Cleaved by Factor D -> C3bBb (C3 convertase)

Positive feedback loop generating > C3b once C3b becomes available

31
Q

What are the 3 outcomes of a C3 convertase being generated?

A
  • anaphylatoxins. eg c3a/c5a. chemoattractants that recruit other phagocytic cells to site of infection eg neutrophils.
  • opsonisation of pathogens. phagocytes w/ c3b receptors destroy & engulf pathogen
  • formation of MAC -> cell lysis
32
Q

Describe how we lyse foreign cells

A
  • formation of Membrane attack complex.
  • complex of C5b - C9 components. C5b, C6, C7 in a complex @ cell membrane. C7 binds to cell membrane. C8 binds & inserts into membrane. C9 polymerises(around 10-16 molecules) and pore formed.
33
Q

What are the 3 main ways that complement activation is regulated?

A
  • components rapidly hydrolysed in fluid phase
  • soluble and membrane bound regulatory proteins eg factor H competes w/ Facto B for C3b binding. C1 inhibitor inactivates C1. carboxypeptidase N inactivates C3a/C5a. CD59 on host cells binds c9 and prevents MAC formation
  • inhibitory regulators facilitate dissociation of the complexes eg DAF, MCP augment dissociation of C4b/C2a OR C3bBb
34
Q

What disease is assocaited w/ deficiency of Factor H?

A

age - related macular degeneration

35
Q

What types of diseases is complement effective against?

A

mainly bacterial, fungal. potentially some viruses

36
Q

How is complement associated w/ adaptive immune system?

A
  • classical pathway
  • aids clearance of immune complexes]
  • role in activating B/T cells
37
Q

Name 2 preformed effector cells.

A

mast cells, macrophages
these exist in tissues eg lungs
all cells posses some level of innate immunity

38
Q

draw a diagram giving an overview of the complement system; from activation to responses

A

word

39
Q

give an example of a preformed effector cell and state its location

A

lung macrophages and mast cells

- already embedded in tissue, act as sentinel cells (defence molceules)

311 - Molecular Immunology (18 decks)

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