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Immunology and Infection > Immune Evasion and Suppression > Flashcards

Immune Evasion and Suppression Flashcards

1
Q

what features does E.coli have that can manipulate the host?

A
  • PAI of genes
  • type 3 secretion system (T3SS)
  • E.coli immodulatory expression: shiga toxin
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2
Q

what is the PAI?

A
  • extra pathogenecity island DNA in pathogenic strain

- encodes toxins, adhesins, sidenophores, immunoe modulatory factors

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3
Q

what is the T3SS?

A
  • pathogen delivery system and its effector molecules to modulate host cell properties
  • about 20 proteins encoded by the PAI
  • like a syringe that injects proteins into the host cell (complex molecular syringe)
    0 can alter host in different ways depending on specific effector proteins
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4
Q

what is the shiga toxin?

A
  • extracellular toxin
  • targets ribosomes
  • inhibits ribosomes and induces the apoptotic pathway
  • bacteria are also competiting with each other
  • HUS - kidney damage
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5
Q

what is helicobacter pylori?

A
  • causes gastric ulcers, can block transcription of T cell growth factor IL-2
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6
Q

what does HIV do?

A

directly attacks the innate immune system, prevents phosphorylation of T cell receptor cascade and prevents formation of immunolgical synapse

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7
Q

how does the HIV affect the immune system?

A
  • presentation of antigens with signalling, viruses can disrupt the formation of this synapse
  • leaves patients with a weakened immune system so they die of secondary infection
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8
Q

what does HIV target?

A
  • mainly targets T cells and macrophages (HIV replication)
  • destroys their function and reduces their numbers
  • HIV attaches to CD4 on the surface of T cells
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9
Q

how does HIV infect macrophages?

A

interaction between viral gp120 with CD4 and CCR5 (co-receptor)

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10
Q

how does HIV effect T cells?

A

interaction between viral gp120 with CD4 and CXCR4

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11
Q

how does T. cruzi prevent T cell activation?

A
  • prevents activation of T-cells by re-sialiation, transfers SA from host cells to parasite surface
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12
Q

how do large extracellular helminths interact?

A
  1. surface molecules

2. secreted molecules

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13
Q

how do helminths not be targeted?

A

give off an elaborate system of chemicals

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14
Q

why does helminth infection correlate with inflammatory disease?

A
  • helminth infection ubiquitous throughout human evolution
  • our immune system has evolved in the presence of worms
  • helminth infection is now rare
  • allergy and autoimmunity
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15
Q

what is the hygeine hypothesis?

A
  • western inflammatory is the direct result of reduced pathogen exposure (including helminths)
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16
Q

how can helminths modify the host with secretory models?

A
  • ‘Excretory/Secretory (ES) molecules
  • produce parasite and modulatory molecules
  • suppress macrophages, B and T cells and dendritic cells
  • in combination with commensal bacteria can bias the host cells and influence inflammations
  • allows worms to prevent/limit immune attack
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17
Q

does worm infection prevent inflammatory disease?

A
  • asthma = allergic lung inflammation
  • induce inflammation in mice, cause acute inflammation
  • infect the mice with worms it completely goes down
  • suggest that intestinal helminth infection prevents lung allergic reaction
  • worm induces regulatory T cells (limit inflammation)
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18
Q

what are the immunosuppressive molecules in helminths?

A
  • want to isolate the molecules the worms are releasing
  • eg TGFB
  • promotes worm survival but prevents western diseases
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19
Q

how do viruses avoid the immune system?

A

devised immunoevasins to block their proteins being present to CD8+ T cells

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20
Q

what is the TAP complex?

A
  • peptide delivery system from the cytosol ER, proteasome delivers peptides which are taken in by the TAP complex to be processed and loaded onto MHC I
  • viruses use molecules to inhibit or block the uptake of peptides so they can’t make it into the ER lumen and can’t be loaded onto MHC I
21
Q

how does herpes simplex avoid the immune system?

A
  • stops peptide binding to TAP

- blocks tapasin

22
Q

how does the bovine herpes virus avoid the immune system?

A
  • inhibits the peptide transport itself, blocks TAP1 and TAP2 from importing
23
Q

what happens if viruses block their own recognition from the immune system?

A

cant be presented by MHC I

24
Q

what are the 2 forms of leishmania taken up by immune cells?

A
  1. promastigote

2. amastigote

25
Q

what is the promastigote?

A
  • immune cells only encounter cell
  • come from the sand fly
  • ones that are human infective won’t divide
  • have to be taken up into the lysosomal environment
  • lysosomal environment has a lower pH and higher temperature which triggers them to become amastigotes
26
Q

what is the amstigote?

A

divide and cause disease

27
Q

how is leishmania infective?

A
  • neutrophil infected by promastigote it presents the antigen to a macrophage and is engulfed
  • attacks macrophages and DCs
  • phagocytes internalise leishmania and then are destroyed
28
Q

how does leishmania affect sandflies?

A
  • have commensal bacteria in their
  • when they transmit their bacteria with the leishmania and saliva it creates an inflammasome activation
  • draws out the immune cells which they can then infect
  • human infection form can also swim towards macrophages
  • when you treat the sand-flys first with antibiotics you dont get the inflammation response and transmission
29
Q

what impact does the surface of parasites of on phagosomes? (leishmania)

A
  • whether the lysosome can fuse with the phagosome
  • whether they can cleave the VAMP8 thats necessary for fusion of phagocytic vesicle
  • can inhibit their own presentation to MHC I cells
30
Q

what is the surface of parasites like? (lesihmania)

A
  • GP63 is on the surface of the metacyclic stage of the parasite
  • once in the parasitic vacuole its theorised that they give off exosomes
  • immunomodulatory factors in them and can shut down translation of host macrophages
31
Q

what happens once the parasite is in the parasitic vacuole? (leishmania)

A
  • bud off parasite
  • fuse with parasitic vacuole
  • go into the cytoplasm of the macrophage
  • can the pH of the lysosome for its own survival
  • they can also flip the mebrane
32
Q

how can leishmania stop microbididal functions?

A

NO, TNFa, ROS

33
Q

how does Lesihmania promote an anti-inflammatory response?

A
  • IL-10 leading to Lesihmania persistence
34
Q

what are the two key proteins on influenza?

A
  • hemagglutinin (attach to host receptors)

- neuraminidase (breaks down sialic acid to allow budding)

35
Q

what are the major serovars in influenza?

A

15 different Ha and 9 different Na

36
Q

what are the two causes of antigenic variation in influenza?

A
  • antigenic drift (minor mutations)

- antigenic shift (major re-assortment)

37
Q

what happens in antigenic shift?

A
  • infected by two flus simultaneously, tend to have an animal associated with them
  • this is how we get pandemics
38
Q

what is the main source of variation in trypanosomes?

A

variation surface glycoproteins (VSGs)

39
Q

what role does VSG have?

A
  • can switch
  • if an antibody lands on a VSG it moves the antibody to its flagella pocket and ingests it and digests it and switches the VSG back on the surfaces
40
Q

how does VSG create antigenic variation?

A
  • many more than 1000 VSG genes on the genome
  • almost all are pseudogenes or gene gragments
  • can create new genes by recombining fragemnts
41
Q

what is the role of PfEMP1 proteins?

A
  • insert into RBCs and develops surface knobs
  • contains the parasite proteins
  • stick to the endothelial lining of blood vessels (dont get cleared by the spleen)
  • become sticky and form blood clots and inflammation
42
Q

what is the strutcure of PfEMP1?

A
  • massive protein complex
  • DBL domains are variable
  • multiple copies of the genes throughout the genome they can recombine
  • PfEMP1 can recombine multiple of the DBL and CIDR domains
  • variable enough that the host never really clears the RBCs
43
Q

what makes T.cruzi difficult to target?

A
  • every stage of T.cruzi is infective
  • infect any nucleated cell
  • do this by triggering their own endocytosis via calcium signalling
44
Q

what are some key points of infectivity of T.cruzi?

A
  • have multiple receptors
  • trigger their own endocytosis
  • once on a parasitic vaciole they have to escape in order to get into the cytoplasm where they differentiate into amastigotes and divide rapidly
45
Q

what is the main surface antigen of T.cruzi?

A

surface trans-sialidases

46
Q

what is the role of trans-sialidases?

A
  • snip off sialic acid off of your normal cells
  • ligate them onto the muscins of the T.cruzi
  • basically disguises the T.cruzi trypamastigote
  • suppression of T cell recognition and internalisation into any cell
47
Q

how does T.cruzi escape the lysosome?

A
  • post phagocytosis - NADPH oxidase - O2 - H2O2 - can be toxic to a parasite
  • T.cruzi peroxidases and superoxide disumtases
  • escape the lysosome to the cytosol
  • do this via TC-TOX (insert this into the membrane)
  • forms multiple pores and rips the parasitic vacuole apart
48
Q

why does T.cruzi need to get to the amastigote stage?

A
  • to divide
  • re-differentiate to trypamastigotes and they’re much larger
  • rip the cell apart
49
Q

what is congenitcal transmission?

A
  • complement can act as a bridge to the trypamastigote
  • triggers phagocytosis
  • tried to block this
  • but this actually promoted uptake of T.cruzi

Immunology and Infection (13 decks)

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