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Biochem > Complement System > Flashcards

Complement System Flashcards

1
Q

define the innate immune system

A

-genetically determined and nonspecific

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2
Q

what are the elements of the innate immune system

A

mucous secretions, complement proteins, and neutrophils, macrophages, and dendritic cells

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3
Q

define the adaptive immune system

A

involves B cells and T cells containing a small number of genetically encoded proteins that combine to produce an enormous variety of proteins capable of recognizing and deactivating anitgens

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4
Q

which immune system do you acquire and which are you born with

A

acquire- adaptive
born with- innate

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5
Q

what are the functions of the complement system

A
  • alters the membrane of pathogens and cellular debris
  • enhance the inflammatory response via release of anaphylatoxins that promote cell activation or migration to an inflammatory site
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6
Q

what does opsonization promote

A

the removal of particles via complement receptors on host cells

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7
Q

what is the function of opsonization

A

leads to assembly of the membrane attack complex on pathogens and lysis

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8
Q

how does the complement system work in innate immunity

A

complement system becomes activated on a target such as apoptotic cells, tissue debris or pathogens

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9
Q

what are the mechanisms in which the complement system works with innate immunity

A

-natural, spontaneous turnover (tick over) of C3 engages the alternative pathway
- binding to the target of naturally occurring antibodies engages the classical pathway
- binding of lectins to carbohydrates on the target engages the lectin pathway

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10
Q

what are natural antibodies replaces with in adaptive immunity

A

specific antibodies

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11
Q

what immune functions does complement trigger

A

phagocytosis
inflammation
membrane attack

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12
Q

how does phagocytosis work in complement

A

by opsonizing antigens. C3b has most important opsonizing activity

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13
Q

how does inflammation work in complement

A

by chemotactically attracting macrophages and neutrophils

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14
Q

how does membrane attack work in complement

A

by rupturing cell wall of bacteria

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15
Q

what is inflammation

A

a local response to cellular injury that is marked by capillary dilation, leukocytic infiltration, redness, heat, and pain
- serves as a mechanism initiating the elimination of noxious agents and of damaged tissue

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16
Q

what happnes in a type 1 allergic reaction

A

swelling is produced by the release of serum into the tissues (wheal) and redness of the skin resulting from the dilation of blood vessels (flare)

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17
Q

what is the classical pathway triggered by

A

activation of the C1 complex
- antigen: antibody complex

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18
Q

how does the lectin pathway start

A

mannose-binding lectin or ficolin binds carbohydrates on pathogen surfaces

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19
Q

what is the mannose-binding lectin pathway homologous to but how is it different

A

the classical pathway but uses opsonins such as MBL and ficolin instead of C1q

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20
Q

what is the alternative pathway activated by

A

at a low level, from the spontaneous C3 hydrolysis due to the breakdown of the internal thioester bond
- pathogen surfaces

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21
Q

what does the alternative pathway not rely on

A

pathogen-binding antibodies like the other pathways

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22
Q

what molecules does the classical pathway use

A

C1q, C1r, C1s, C4, C2

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23
Q

what molecules does the lectin pathway use

A

MBL/ficolin, MASP-2, C4, C2

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24
Q

what molecules does the alternative pathway use

A

C3, B, D

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25
Q

what does C3 convertase do

A

cleaves C3 into C3a and C3b

26
Q

what do C3a and C5a do

A

they are peptide mediators of inflammation, phagocyte recruitment

27
Q

what does C3b do

A

binds to complement activators of phagocytes, opsonizes pathogens and removal of immune complexes

28
Q

what do C5b, C6, C7, C8, and C9 do

A

MAC, lysis of certain pathogens and cells

29
Q

what does the classical pathway of complement involve the cleavage of

A

C2 C4 and C3

30
Q

what is the C1 complex made of

A

C1q C1r and C1s

31
Q

describe C1q

A

composed of 6 identical subunits with globular heads and long collagen-like tails. the tails combine to binds to two molecules each of C1r and C1s to form the complex

32
Q

what is the opsonization mechanism

A
  • activated C1s cleaves C4 to C4a and C4b which binds to microbial surface
  • C4b then binds C2 which is cleaved by C1s to C2a and C2b forming the C4b2a complex
  • C4b2a is an active C3 convertase cleaving C3 into C3a and C3b which binds to microbial surface or to the convertase itself
  • one molecule of C4b2a can cleave up to 1000 molecules of C3 to C3b. many C3b molecules binds to the microbial surface
33
Q

what does mannan binding lectin form a complex with

A

serine proteases that resemble the complement C1 complex

34
Q

describe the MBL complex

A

forms clusters of 2-6 carbohydrate binding heads around a central collagen stalk. MASP1 and MASP2 are associated with the complex

35
Q

what is another term for C4b2a and what does it lead to

A

C3 convertase, leads to the generation of C5 convertase

36
Q

what does C5 convertase do

A

cleaves C5 into C5a and C5b

37
Q

what pathways share the same biological activities and the same regulatory proteins

A

the lectin pathway and the classical pathway

38
Q

what is the mechanism of the alternative pathway

A

-C3b deposited by classical or lectin pathway C3 convertase to a pathogen or cell surface
-C3b binds factor B
- bound factor B is cleaved by plasma protease factor D into Ba and Bb
- C3bBb complex is a C3 convertase cleaving many C3 molecules to C3a and C3b

39
Q

what does C3b lead to

A

the MAC complex

40
Q

what forms the pore on membrane surface

A

C9

41
Q

how is the MAX complex pore formed (mechanism)

A

-C5b binds to C6 and C7
- C5b67 complexes binds to membrane via C7
- C8 binds to the complex and inserts into the cell membrane
- C9 molecules binds to the complex and polymerize
- C9 binds each other to form a pore in the membrane

42
Q

how does opsonization and phagocytosis occur via activation of complement

A

-C3b is deposited on surface of the microorganism by MBL and/or alternative pathway
- C3b binds to CR1 on the surface of phagocytes
- C5a binds and activates the cell to phagocytose microorganisms

43
Q

what step do the alternative pathway, lectin pathway and classical pathway converage at

A

C3 convertase

44
Q

what regulates complement activation

A

a series of proteins that act on different stages of the complement cascade, dissociating the complex or catalyzing the degradation of complement proteins

45
Q

what regulates the alternative pathway C3 convertase

A

DAF, CR1, MCP, and factor H

46
Q

what does DAF do

A

displaces Bb from C3b and C2b from C4b thereby preventing C3 convertase

47
Q

what does MCP do

A

dissociates C3 convertases and factor 1cleaves

48
Q

what is paroxysmal nocturnal hemoglobinurina

A

acquired disorder that results in premature death and impaired production of blood cells

49
Q

what blood cells does PNH effect

A

RBCs, leukocytes, and platelets

50
Q

who is usually affected by PNH

A

both sexes equally diagnoses in young adulthood

51
Q

what is the mechanism of PNH

A

deficiency in DAF protein

52
Q

what does Eculizumab do and what is it used for

A

used for PNH and blocks C5 convertase

53
Q

what is atypical hemolytic uremic syndrome

A

results from chronic uncontrolled activation of the complement system

54
Q

what happens in atypical hemolytic uremic syndrome

A

mutliple blood clots form throughout body in small blood vessels which can lead to stroke, heart attack, kidney failure, and death

55
Q

what is the mechanism of atypical hemolytic uremic syndrome

A

mutations in factor H, factor I, or membrane cofactor protein

56
Q

what is the most common functional defect in atypical hemolytic uraemic syndrome and age related macular degeneration

A

reduced cofactor activity (MCP or factor H) for C3b

57
Q

what is hereditary angioedema

A

recurrent attacks of severe swelling

58
Q

what is the type 1 form of hereditary angioedema

A

deficiency of C1

59
Q

what is the type 2 form of hereditary angioedema

A

an atypical C1 protein that is less capable of suppressing activation of the complement system

60
Q

what is type 3 form of hereditary angioedema

A

due to mutations in factor 12 gene

61
Q

what is the mechanism of C1 inhibitor deficiency in hereditary angioedema

A

factor 12a and plasmic cause prekallifrein to be converted into lakkikrein which converts high molecular weight kininogen to bradykinin which results in vasodilation, smooth muscle contraction and edema

Biochem (34 decks)

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