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Zach- Immunology > Lecture 4-2, complement system > Flashcards

Lecture 4-2, complement system Flashcards

1
Q

What functions will the complement system work to achieve?

A
  1. opsonize microbes
  2. recruit phagocytes
  3. possibly directly kill microbe
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2
Q

What are the different pathways that can be activated in the complement system?

A
  1. alternative pathway
  2. classical pathway
  3. lectin pathway
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3
Q

What does the complement system work in cooperation with what other proteolytic cascades?

A
  1. blood coagulation pathways

2. kinin-kallikrein system that regulates vascular permeability

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4
Q

Early step 1 of complement activation forms what?

A
  • C3 convertase complexes form C3a and C3b, which produce inflammation and opsonize microbes respectively
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5
Q

Early step 2 of the complement activation forms what?

A

C5 convertase, which forms C5a and C5b. Start inflammation and start the late steps

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6
Q

What is the late step of complement activation pathway?

A

form MAC to punch holes into the microbial membranes

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7
Q

What is a strong chemoattractant that can induce changes to blood vessel permeability?

A

soluble C5a

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8
Q

What is required to activate the classical complement pathway?

A
  1. IgM, IgG and C1q,r,s complex
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9
Q

What forms the C3 convertase in the classical pathway?

A

C4b and C2a

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10
Q

What forms C5 convertase in the classical pathway?

A

C4b, C2a, C3b

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11
Q

Is the classical system considered innate or adaptive in nature?

A

not innate, as an Ab is required in order to activate

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12
Q

Of the three pathways which one is the most sensitive? The least?

A
  1. Classical

2. Alternative

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13
Q

How is the Lectin pathway activated?

A
  1. MBP binds with bacteria and activates MASPs which then contribute to the formation of C4b and C2a
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14
Q

How is the alternative pathway activated?

A

C3 undergoes spontaneous hydrolysis and combines with factor B and D to form C3b and Bb

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15
Q

What forms C3convertase in the alternative pathway?

A

C3b and Bb

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16
Q

What forms C5 convertase in the alternative pathway?

A

C3b, Bb, C3b

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17
Q

What is unique about the alternative pathway?

A

It can activate C5 convertase, by contacting an organism and also form an amplification loop.

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18
Q

What is required in order to produce the C3b and Bb complex?

A

Factor D

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19
Q

If properdin is present, what happens when C3b, Bb is formed?

A
  1. complex C3b, Bb, P is formed which forms an amplification loop to activate more C3b
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20
Q

If no properdin is present, what is formed in the alternative pathway?

A

The C3b, Bb complex will combine with another C3b, complex to form C5 convertase and induce the MAC

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21
Q

How is the lectin pathway activated?

A

1.mannose binding lectin, recognizes and binds with terminal mannose residues on microbial glycoproteins or glycolipids

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22
Q

What is the major role of MBL?

A

these mediate and active that pathway of when an Ag is present. What happens with too many/too few?

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23
Q

How do Sp-A and SP-D operate or act as?

A

similar to opsonins, that are located in the alveoli

-inhibit bacterial growth, can activate macrophages

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24
Q

What is ficolin and what does it bind with?

A
  1. similar to mannose binding lectin

2. binds N-acetylglucosamine to activate MASP1-2

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25
Q

What type of molecule is ficolin?

A

humoral molecule of innate immune system

26
Q

When ficolin bind to bacteria what is the result?

A
  1. limit infection and direct adaptive immunity response via opsonization
  2. initiate lectin pathway by activating MASP1-2
27
Q

Which complex forms the pore of the MAC?

A
  1. C9
  2. C5b, 6, and 7 bind to PM via C7
  3. C8 also binds and anchors into the PM
28
Q

How is the complement system useful in attacking microbes but not our own mammalian cells?

A

mammals express regulatory proteins that inhibit, destroy the convertases, and therefore can’t signal them for the formation of MAC

29
Q

What does the decay accelerating factor do? (DAF)

A

blocks the C2:C4 interaction

can also cause dissociation of C4b:C2a complex

30
Q

What does complement receptor 1 (CR1) do on mammalian cels?

A

cause dissociation of C4b:C2a complex

also cleaves the C4b and C3b

31
Q

What does factor I (FI) do on the surface of mammalian cells?

A

cleaves the C4b and C3b

32
Q

What do products C5a, and C3a help to initiate?

A

produce inflammation at the site, and will therefore attract leukocytes

33
Q

In what ways are tissue macrophages activated?

A
  1. CD40 ligan and IFN-gamma (t lymphocyte stimui)

2. chemotaxis of tissue repair/fibrosis

34
Q

If tissue macrophages are activated what will this activate?

A

synthesis of proteins

35
Q

What cytokines act on local leukoctyes and endothleium to produce inflammation?

A

TNF and IL-1

- both will cause expression of IL-6

36
Q

What cytokines are responsible for fever, acute phase protein synthesis and increased lymphocyte production?

A

TNF, IL-1, IL-6

37
Q

What pathologic abnormalities can systemic TNF release cause?

A
  • decreased cardiac function
  • thrombosis/capillary leakage
  • metabolic abnormalities from insulin resistance
38
Q

What are Acute Phase Proteins (APP) from the pentraxin family?

A
  1. C-reactive protein

2. serum amyloid

39
Q

The increased level of CRP and SAP comes from where, which is under the influence of IL-1 and IL-6?

A

the liver

40
Q

CRP recognizes what PM structure?

A

phosphorylcholine

41
Q

SAP recognizes what PM structure?

A

phosphatidylethanolamine

42
Q

Where are Type I interferons produced (IFN-alpha/beta)

A

virus-infected cells

43
Q

What happens when IFN-alpha/beta bind uninfected cell?

A

a JAK-STAT signaling pathway is activated which produces proteins to interfere with viral replication

44
Q

What happens when IFN-alpha/beta bind infected cells?

A

cause the expression of genes the enhance the susceptibility to CTL-mediated killing

45
Q

TNF is a cytokine mediator for what?

A

acute inflammation of bacteria and other infectious microbes

46
Q

What two components are able to cause TNF production?

A

PAMPs and DAMPs

pathogen and damage/danger associated molecular patterns

47
Q

Which receptors activate the NF-kB transcription factor, and produce what with that activation?

A
  1. TLR, NLR, RLR

2. ultimately produce TNF expression

48
Q

Production of IL-1 generally requires two signals, that are what?

A
  1. activation of new gene transcription

2. activation of inflammasomes

49
Q

What structures generate the IL-6 in response to PAMPs?

A
  1. mononuclear phagocytes
  2. vascular endothelial cells
  3. fibroblasts
  4. cells responding to IL-1
50
Q

What cells secrete IL-12?

A
  1. DC

2. macrophages

51
Q

What does IL-12 do when released?

A
  1. generate IFN-gamma production from NK and T cell

2. promotes differentiation of Th1 cells which defend against intracellular infection

52
Q

What is IL-18 used for?

A
  1. enhances function of NK cells

2. production is based on activation of inflammasome

53
Q

What is IL-15 used for?

A
  1. growth stimulating and survival for NK and CD8+ T cells
54
Q

When TLR receptors are activated by a microbe, what do macrophages release, and what does this cause in the body?

A
  1. TNF, IL-1, IL-6, IL-2

2. produces inflammation and activates the adaptive immune resposne

55
Q

If cytokine receptors are activated by IFN-gamma, what type of response does the activated macrophage produce?

A
  1. kill microbes via use of ROS and NO

2. still also able to generate a inflammatory response with IL-6, IL-2, IL-1, TNF

56
Q

Which cytokines are responsible for inducing fever in people?

A
  1. TNF and IL-1

2. IL-1 has a stronger response, and is most responsible

57
Q

How do TNF and IL-1 generate the production of a fever?

A
  1. increase the production of prostaglandins in hypothalamic cells
58
Q

What do medications, like aspirin, do to combat fever?

A
  1. block the action of cytokines (TNF, IL-1) and prevent prostaglandin synthesis stimuli
59
Q

What does TNF do to produce hypotension or shock?

A
  1. inhibits myocardial contractility and vascular smooth muscle tone
60
Q

What is the effect of prolonged production of TNF?

A
  1. cachexia: necrosis of muscle and fat cells

2. caused by appetite suppression and reduced levels of lipoprotein lipase.

Zach- Immunology (10 decks)

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