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IMMUNOLOGY VDMP817 > lecture 7 > Flashcards

lecture 7 Flashcards

1
Q

zymogens

A

pro enzymes
components exist as this
highly conserved bw specifies

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2
Q

complement system initiated through 4 distinct pathways

A

w identical end results

  1. classical
  2. alternative
  3. MBL
  4. C2 bypass pathway: intracellular activity
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3
Q

complement system plays a role in both

A

innate and adaptive immunity

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4
Q

complement proteins secreted in Liver by Macrophages as

A

zymogens and are found in normal serum

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5
Q

innate pathway

A

includes alternative and lectin pathways

activated by recognizing PAMPS

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6
Q

adaptive pathway

A

includes classical pathways

activated by presence of antibody bound to antigen

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7
Q

complement components (C3b) bind

A

covalently to invading microbes and opsonize them

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8
Q

membrane attack complex

A

complement components that punch holes in microbes

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9
Q

chemoattractants trigger

A

inflammation through C3a C5a

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10
Q

deficiences of some components can lead to

A

increased susceptibility to infections

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11
Q

major proteins designated as

A

C1-C9

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12
Q

lectin pathway

A

triggered by mannose-binding lectin - MBL
revognizes mannose on microbial glycoproteins and glycolipids
uses C4 & C2
creates C3 components (C3b and C3a)
C3 deposited on microbe and opsonization/phagocytosis starts
C5 converts to C5a and b - comes in and form attack on membrane

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13
Q

C3a

A

inflammation

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14
Q

C5a

A

inflammation

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15
Q

alternative pathway

A

triggered by direct recognition of certain microbial surface structures (ex: spontaneous cleavage of thioester bond in C3)
B and C3
creates C3a and b components which generate C5a and C5b
attack on membrane by complement proteins!

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16
Q

classical pathway

A

uses C1 protein to detect IgM, IgG1, or IgG3 antibodies bound to the microbe
uses C4 and C3
creates C3a and b components which generate C5a and C5b
attack on membrane by complement proteins!

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17
Q

MAC formation

A

C6 + C5b + C7 + C8 binds C9 units together to make membrane attack complex to cause cell lysis
initiated by lectin, alternative and classical pathways

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18
Q

C1q

A

complement activating protein

binds w C1r2s2 onto microbial surface antigen bound to IgM antibody

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19
Q

mannose binding lectin

A

complement activating protein

binds MASP1/2 to mannose on microbe surface

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20
Q

MASP

A

MBL- associated serine protease

21
Q

Ficolin

A

complement activating protein

binds MASP1/2 to N acetylglucosamine on bacterial cell wall

22
Q

mannose binding lectin

A

complement initation mechanisms
mannose binding lectin (MASP1/2) binds mannose/similar sugars on bacteria, fungi, protozoa & viruses -> conformational change -> C4 and then C2 cleavage -> generates C4a + C2a -> generate C4bC2b convertase -> cleave C3 -> makes C3a + C3b

23
Q

antibodies as complement initiation mechanism

A

antibodies bind to epitopes on pathogens surface -> conformational change -> C1q (like MBL) binds to complement binding site on antibodies w C1r & C1s which are serine proteases -> C4 & then C2 cleavage -> make C4a + C2a -> generate cell bound C4bC2b convertase -> cleaves C3 -> makes C3a + C3b

24
Q

C1r & C1s

A

serine protease - cuts C4 and C2

25
Q

spontaneous C3 cleavage as complement initation mechanism

A

C3 spontaneous breakdown -> C3b + C3a -> C3b surface bound -> a. normal circumstance (no avtivating surfaces) -> Hv binds and creates C3bH -> I inactivates C3b
b. in presence of activating surface B binds to create C3bB -> D acts on it and makes C3bBb + C3bBa -> P acts on it and makes C3bBbP

26
Q

C3 convertases as complement initiation mechanism

A
  1. C4b2b

2. C3bBb

27
Q

C5 convertases as complement initation mechanism

A
  1. C4b2b3b

2. C3bBb3b

28
Q

regulation of complement activation

A

C1, decay accelerating factor (DAF) (CD55), CD59, factor H and I

29
Q

C1 inhibitor

A

disrupts C1 and the classical pathway

30
Q

decay accelerating factor

A

DAF, CD55

dissociates C3 convertases and lectin pathway

31
Q

factor H and I

A

destroy C3b on sialic acid experssing cells

disrupts alternative pathway

32
Q

CD59

A

blocks C9

prevents C5b678 + poly C9 so no MASP or membrane attack

33
Q

C3b and sialic acid

A

C3 breaks down spontaneously into C3a and C3b, if it is bound to sialic acid factor H will bind to C3b
-> activates factor 1 which creates a complex that degrades C3b -> a. iC3b b. C3c and C3d

C3c, C3d and iC3b are opsongens that are unable to initiatiate complement pathway

34
Q

CR1

A

CR1 + C3b in RBC, monocytes, macrophages, neutrophils and T cells

immune adherence receptor
removal of C3b opsonized immune complexes by liver
neutrophil phagocytosis
inhibition of classical and alternative pathways

35
Q

CR2

A

CR2 + iC3b/C3d (g) in B cells

enhances B cell immunity

36
Q

CR3

A

CR3 + iC3B dimer in NK cells, monocytes, macrophages, neutrophils and T cells

adherence receptor
cell-cell interaction and binding
phagocytosis
leukocyte trafficking and migration
outside in signaling
promote inflammation
37
Q

CR4

A

CR4 + iC3b dimer in neutrophils, NK cells, monocytes, macrophages, dendritic cells

same as CR3
adherence receptor
cell-cell interaction and binding
phagocytosis
leukocyte trafficking and migration
outside in signaling
promote inflammation
38
Q

consequences of complement activation

A
  1. complement mediated cytolysis
  2. opsonization and phagocytosis
  3. stimulation of inflammatory reactions
  4. regulate B cell responses
39
Q

complement mediated cytolysis

A

binding of C3b to microbe surface and activate late components of complement
formation of MAC
osmotic lysis of microbe

40
Q

opsonization and phagocytosis of complement activation

A

binding of C3b (or C4b) to microbe - opsonization
recognition of bound C3b by phagocyte C3b receptor (CR1)
phagocytosis of microbe!

41
Q

stimulation of inflammatory responses as result of complement activation

A

proteolysis of C3, C4, C5 to release C3a, C4a, and C5a
recruitment and activation of leukocytes by C3a, C4a and C5a
microbe is DESTROYED by leukocytes

42
Q

B cell responses regulated as consequence of complement activation

A

C3d bound to antigen, binds to BCR and CR2
C3b cleaved by factor 1
C3c + C3d regulate B cell responses

43
Q

complement deficiencies

A
  1. canine C3

2. procine factor H

44
Q

canine C3 deficiency

A

brittany spaniels
autosomal recessive C3 deficiency
experience recurrent sepsis, pneumonia, wound infections - recurrent bacterial infections
organisms: clostridium, pseudomonas, e coli, klebsiella species
treatment: antibiotics and monitoring

45
Q

porcine factor H deficiency

A

yorkshire pigs
factor H inactivates C3b -> prevents excessive alternative pathway activation
autosomal recessive deficiency
renal failure at early age (glomerulonephritis)
treatment: infusion of normal swine serum

C3 will deposit in glomerulus - causing renal failure

46
Q

Neisseria meningitides

A

resistance to complement activation (alternative pathway)

mechanism of immune evasion: sialic acid expression inhibits C3 and C5 convertases

47
Q

streptococcus

A

resistance to complement activation (alternative pathway)

mechanism of immune evasion: M protein blocks C3 binding to organism, and C3b binding to complement receptors

48
Q

evasion of innate immunity by microbes

A
  1. salic acid expression
  2. M protein block
  3. capsule preventing interation w C3b
  4. some bacter inactivate C3a and C5a
  5. produce molecules that mimic regulatory proteins

IMMUNOLOGY VDMP817 (22 decks)

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