innate immunity and inflammation Flashcards

1
Q

different types of PRR
1) phagocytosis

A

some PRRs are pahgocytosis receptors

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2
Q

different kind of PRR
2) cytokine production (TLR)
what does TLR-4 recognise?

A

some PRR are toll like receptos
TLR+PAMP= cell activation and cytokine production
-recognises LPS.
-

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3
Q

what are cytokines?
-how do responsing cells recognise cytokine

A

small soluble proteins rapidly secreted by one cell that can alter behaviour or properties of cell or another cell
-respoding cells carry a specifc receptor

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4
Q

what cells are the first responders of the immune system

A

neutrophils

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5
Q

what are chemokines
-what are they secreted by
-how do responding cells recognise chemokine

A

family of small cytokines that can promote chemotaxis.
secreted by cells of immune system but also stromal cells.
responding cells carry a specific receptor that recognises the chemokine

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6
Q

what do chemokines do?

A

released at sight of injury or insult.
forms gradients
cells expressing corresponding receptor can respond to the chemokine by moving towards signal

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7
Q

how to cytokines activate immune cells
-what cell does this occurs on

A

TNFα binds to TNFR1
on neutrophils

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8
Q

consequence of increased vascular permeability

A

proteins in the blood fluid
-coagulation factors
complement

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9
Q

what does the complement cascade do
1) C3a, C5a ‘anaphylatoxins’
2) C3b
3) C5b-9/ MAC punches holes in membrane of pathogens

A

the complement cascade is a group of proteins working together to destroy pathogens. chain reaction where the activation of one protein leads to the activation of the next.
marks cells by phagocytsis is early signs of infection
1) vascular permeability (inflammation) and recruits more cells to the infection site ‘chemotaxis’.
2) increase phagocytosis by ‘opsonisation’
3) lyses bacteria

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10
Q

the effects of anaphylatoxins in the complement cascade

A

similar to cytokines and histamine. it contributes to vasodilation and mediate chemotaxis

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11
Q

the two different ways to start the activation of complement cascade, and the end result
1) classical (part of adaptive). what happens, what early complenet is recruited, what does it trigger.

2) alternative (apart of innate). what spontaneous breakdown happens, what level does it occur and why.

A

1) binding of antibody to pathogen antigen. recruit early component pathogens (C1). only happens if there are antibodies that bind to pathogen. triggers cascade of protein activation.

2) spontaneous breakdown of C3. deposit of C3b on pathogen surface. happens during every infection with a pathogen. and at a low level to amplify immune response

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12
Q

for both systems what is the key event.
how do they differ

A

key event is the generation of C3 convertase, which cleaves C3 into C3a and C3b
both pathways have different ways of cleaving C3 into C3a and C3b

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13
Q

The cascade ultimately leads to the activation of C3, which is central to the cascade and is involved in all three pathways. This leads to:
-C3a
-C3b
-MAC

A

C3a= promotion of inflammation which attracts more immune cells to the area
C3b= oponisation of pathogens. makes it easier for immune cells to engulf and kill them by pahgocytosis. promotion of inflammation which attracts more immune cells to the area

MAC- kills pathogen

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