the innate immune response Flashcards

1
Q

the innate immune system is (3)

A

non specific, immediate , no immunological memory

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2
Q

adaptive immune system (3)

A

specific to antigen, lag time from exposure to response, immunological memory after exposure

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3
Q

innate humoral

A

complement, enzymes, cytokines

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4
Q

innate cellular

A

phagocytes, natural killer cells, pattern receptors

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5
Q

adaptive humoral

A

antibodies and cytokines

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6
Q

adaptive cellular

A

T cells and B cells

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7
Q

many circulatory but there are some important exceptions

A

M cells, alveolar macrophages

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8
Q

phagocytes are

A

professional kill cells

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9
Q

professional phagocytes

A

monocytes, macrophages, neutrophils, tissue dendritic cells and mast cells

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10
Q

bacteria taken up by endocytosis are destroyed within a

A

phagosome

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11
Q

process of phagocytosis

A

1) microbe is extracellular 2) endocytosis 3) phagosome formation 4) lysosome fusion 5) phagolysosome 6) release of end products into the cell
7) release of end products pit of the cell

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12
Q

the pH of the phagolysosome

A

decreases

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13
Q

three categories o PRRs that can be engaged during phagocytosis

A

1) those that mediate phagocytosis
2) those that initiate inflammatory signal transduction
3) those that do both

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14
Q

mannose receptor

A

a prototypical receptor for PRRs that mediate phagocytosis but does not initiate an inflammatory response

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15
Q

what use mannose receptors

A

virulent strains of mycobacterium tuberculosis e.g. when dormant for a long time- no inflammatory response

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16
Q

some bacteria ave evolved strategies to survive within macrophages e.g. L.pneumophilia

A

won’t progress pass an early endosome

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17
Q

some bacteria ave evolved strategies to survive within macrophages e.g. S.typhimurium

A

won’t progress into a phagolysosome

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18
Q

some bacteria ave evolved strategies to survive within macrophages e.g. F.tularensis

A

will not progress into a phagolysosome and can escape replicate in cytoplasm

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19
Q

some bacteria ave evolved strategies to survive within macrophages e.g. M.tuberculosis

A

won’t progress into late endosome

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20
Q

Mechanism for counteracting these strategies and recognising bacteria in vesicles

A

toll like receptors

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21
Q

nod like receptors (more than 20 have been described)

A

have nucleotide binding oligomerization woman and a number of LRRS

22
Q

LRRs

A

Leucine rich repeats

23
Q

how does listeria moncytogenes counteract recognition and killing

A

can escape from the vacuole to the cytoplasm by action of Listeriolysin- a cholesterol dependent cytolysin

24
Q

how does salmonella counteract recognition and killing

A

use the TLRs to ensure they get to a protective niche and then secrete proteins into the cell to prevent further damage

25
how do the proteins secreted by salmonella protect it from damage
help maintain the integrity of the SCV (salmonella containing vesicle) and its localisation near the golgi of host cells- modulating the host cytoskeleton and interfering with immune signalling
26
how does shigella flexneri counteract recognition and killing
evades degradation in macrophages by inducing their cell death- bacteria are released and inane epithelial cells from the basolateral side
27
mycobacterium tuberculosis phagosome characterised by
- paucity of vacuolar H+ATPase - subsequent inefficient luminal acidification - inadequate levels of mature lysosomal hydrolyses
28
macrophages death cause by secretion
T3SS effectors- recognised by NLRs (Ipaf0 leading to pyropotosis)
29
pyropptosis
a form of necrotic cell death that is associated with rapid plasma membrane rupture
30
autophagy
targets portion of cytoplasm, damaged organelles and proteins for lysosomal degradation and has crucial roles in development and disease
31
how does it start and how is bacteria evolved to cope with this?
1) a cup-shaped membrane sac called the isolation membrane starts to form 2) the isolation membrane elongates and closes to form a double membrane vesicle called the autophagosome 3) the outer membrane of the autophagosome fuses with a lysosome to form an autolysosome 4) leading to degradation of the cytoplasmic contents inside the autophagosome
32
xenophagy
autophagy targeting intracellular pathogens
33
mitophagy
autophagy of damaged mitochondria
34
aggrephagy
autophagy of protein aggregates
35
which genes are responsible for autophagy
LC3- mammalian homologue of ATG8 genes
36
LC3
a mammalian homologue of ate*
37
what appears to function as a tag for autophagy mediated degradation
polyupiquitation , via the ubiquity-proteasime system (aos0 the hallmark of protein degradation)
38
remnants from shigella flexneri that escape
trigger autophagy
39
what can repress autophagy
Type III secretion system effector-n IcsB
40
autophagy in Listeria infection
two pathways: persistent infection and successful fusion with lysosome
41
autophagy in Burkholderia pseudomallei infection
three scenarios happen- look at notes
42
methods of inactivation: Listeria monocytogenes
produce LLO- helps them enter the cell and then escape the phagosome. Then listeria can develop a cytoskeletal body which helps it propel itself into adjacent cells
43
methods of inactivation: salmonella
TLR signalling is required for virulence
44
salmonella- TLR2/4
if present, known as TLR signalling. Prevent acidification of SCV--> inducing virulence genes, which maintain integrity of scv
45
if there is no TLR
pH can be reduced and no salmonella replication
46
what does shigella flexneri use to force entry
TTSS
47
methods of inactivation: Mycobacterium tuberculpsos
small no. of H ATPase. meaning insufficient luminal acidification--> inadequate levels of mature lysosomal hydrolases
48
LC3
triggers autophagy by recruiting phagosomal membrane
49
ubiquitation
is a key determinant of protein fate by tagging proteins for proteasomal degradation
50
membrane reputed by LLO..
seem to recruit autophagy machinery
51
scenarios of autophagy of Burkholderia
1) phagosome and lysis 2) phagosome escape- builds tail and escape 3) phagosomal escape and then autophagy starts again- lysis