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II > L1.3 Regcosing the pathagens > Flashcards

L1.3 Regcosing the pathagens Flashcards

1
Q

2 immune systems

A

innate and adaptive systems

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2
Q

3 types of barriers

A

-mechanical, chemical, biologic

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3
Q

components of innate immune system (IIS)

A

humoral components like plasma proteins and cellular like WBCs

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4
Q

3 types of WBC

A

lymphocytes, monocyte and granulocytes

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5
Q

3 types of lymphocytes

A

T,B and NK cells

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6
Q

3 types of tissue cells

A

macrophage, MAST and dendritic cell

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7
Q

types of pathogens

A

bacteria, protozoan, worms, flukes, fungi, virusus

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8
Q

what do we have to regconsice pathagens AGs

A

pattern recognition receptors (PRRs)

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9
Q

scienctic name for antigens

A

pathogen associated molecular patterns(PAMPs)

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10
Q

which cells has a lot of PRRs

A

all tissue cells

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11
Q

what are TLRs

A

PPRs expressed on the surface of the phagoctyic cells

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12
Q

how many TLRs

A

6

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13
Q

how to recognise exposed nucleic acids from a pathogen

A
  • the nucleic acid taken up inside

- TLR-4 recgonise the NA

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14
Q

what type of PRR can detect pathogenic sugars

A

CLR on the surface of the macrophages and dendritic cells

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15
Q

whats the cell response after TLR is bound to the pathogen

A

inflammation, interferon and adaptive immunity (get rid of infection )

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16
Q

pathway of inflammation activation

A

TLR triggers release of NFkB,

  • triggers release of proinflammatory cytokines/chemokines
  • triggers inflammation and releases IL1, IL6, IL8 and TNFa
17
Q

what are interferon

A

molecules that inhibit viral DNA replication by stopping protein synthesis and degrading mRNA

18
Q

signs of infection

A

PAMPS leads to pain, redness, heat and swelling

19
Q

why does blisters have no infection

A

there was physical damage to tissue cells

- so there was some necrosis

20
Q

what are DAMPs

A

damage associated molecular patterns
-they are danger signals
-

21
Q

what DAMPs can be released

A
  • mitochondria
  • ATP
  • histones
  • nucleic acids
22
Q

how is pus formed

A

enzymes released by neurcotic neutrophils

- promotes inflammation

23
Q

role of NK cells

A

kill infected and cancer cells

24
Q

how many set of receptors of NK cells

A

2

-inhibitory and activatory

25
Q

how does NK cell recongise and not kill normal cell

A 
NK inhibitory receptor binds to MHC class I on normals
- stop signals from activatory receptors
26
Q

how does NK cell recnoginse pathogenix cell

A 
no MHC class 1 so the activatory receptor bind to a antigen on the pathogenic cell
- NK triggered to kill it by inducing apoptosis
27
Q

how does a dendritic cell get activated

A

pathogen and antigen taken up by the cell

  • expresses peptide MHC complex on the surface
  • gets activated and migtrates to where it meets T cell to present the antigen
  • then T and B cells starts to proliferate
  • this is adaptive immunity
28
Q

what is complement system

A

part of IIS, helping ABs to kill bacteria by using proteins

29
Q

what are complenment proteins

A

pro enzymes that has 2 fragment s

30
Q

role of small fragment of Complement porteins

A

mediator of inflammation

31
Q

role of large fragment of Complement porteins

A

activates the next proenzyme and binds to microbe surface

32
Q

3 pathway of complement activation

A

-lectin, classical, alternative

33
Q

when does all 3 complement activation pathways converge

A

to form C3 convertases for C3 and C5

34
Q

what are the consequences of the complement system

A

opsonisation, lysis and inflammation

35
Q

how does C3b help opsonisation

A

C3b bind to the bacterial wall

  • C3b then bind to thr CR1 (complement receptors) on phagocytes
  • triggers phagoctyosis
36
Q

what is membrane attack complex

A

they bury themselves into the bacteria’s surface and cause holes. This cause lysis of the surface

37
Q

actions of C3a and C5a

A

activate tissue mast cells and endothelial cells

- attract innate immune cells to the infection site

II (21 decks)

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