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LECOM Microbiology MS1 > Complement (Exam 1) > Flashcards

Complement (Exam 1) Flashcards

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1
Q

Where are complement proteins primarily produced

A

liver
spleen
macrophages

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2
Q

What do complement components consist of

A

Proteins C1-C9
Factors B, D, and P
Numerous inhibitors of the pathway

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3
Q

What are the two proteolytic fragments seen in complement

A

B fragment

A gragment

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4
Q

Generally B fragment is what

A

larger and biologically active

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5
Q

Generally A fragment is what

A

smaller, not biologically active

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6
Q

What is needed to induce a classical complement pathway

A

antibody bound to specific antigen on pathogen surface

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7
Q

What is needed to induce alternative complement pathway

A

pathogen surface creates local environment conducive to complement activation

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8
Q

What will occur in all 3 complement pathways once activated

A

induces inflammation
lyse certain infectious agents
opsonize infectious agents
clear immune complexes

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9
Q

What is activated by all three complement pathways

A

C3

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10
Q

What complement pathway involves antibodies and what antibodies are involved

A

classical

IgG and IgM

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11
Q

Which of the complement pathways are involved in innate immunity

A

Lectin and alternate

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12
Q

Which of the complement pathways are involved in adaptive immunity

A

classical

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13
Q

What initiates the alternate pathway

A

spontaneous lysis of C3 causing C3b to bind and initiate pathway

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14
Q

What complement proteins are common to both alternate and classical pathways

A

C3b, C3a, C5a, MAC

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15
Q

How many molecules of IgG and IgM need to be bound to C1 to initiate classical pathway

A

1 IgM

2 IgG

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16
Q

What form are IgG and IgM secreted in

A

IgG: monomer
IgM: pentamer

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17
Q

What is needed to form C3 convertase

A

C4b and C2a

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18
Q

Briefly outline the process in which C3 is cleaved into proteolytic fragments

A

C4 is cleaved into C4a and C4b—C4b binds to surface

C2 is then cleaved into C2a and C2b. C2a binds to C4b to create C3 convertase

C3 is converted to C3a and C3b. C3b remains on cell surface

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19
Q

What classes are C3b and C3a

A

C3b opsonin

C3a anaphylotoxin

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20
Q

What are the functions of C5a and C5b

A

C5a: anaphylotoxin and chemotaxis
C5b: initiates MAC formation

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21
Q

What must be present to form C5 convertase

A

C4b, C2a, C3b

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22
Q

What protein is inadequate in a MAC deficiency

A

any protein from C5-C9

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23
Q

Which type of fragment will acquire enzyme activity

A

B fragments

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24
Q

What are the a fragments of complement known as

A

anaphylatoxins

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25
Q

What complement effector is involved in opsonization

A

C3b

26
Q

What does C3b bind to

A

pathogen to help the phagocyte opsonize more efficiently

27
Q

What complement effector is involved in clearance of immune complexes

A

C3b

28
Q

What complement effectors are chemotactic

A

C3a and C5a

29
Q

What complement effectors are part of the membrane attack complex

A

C5-C9

30
Q

What are the opsonins

A

C3b and IgG

31
Q

What is opsonization

A

antibody binds to antigen on bacteria via IgG and goes to a phagocyte

32
Q

What receptors does opsonization occur through

A

complement receptors

33
Q

What do immune complexes trigger

A

type 3 hypersensitivity reactions and inflammation

34
Q

How are immune complexes made soluble

A

C3b disrupts the complexes to make them soluble

35
Q

What role do RBCs play in clearance of immune complexes

A

C3b on immune complexes can bind to the C1 receptor on RBCs and be taken to the liver and spleen where they will be removed

36
Q

When will antigen and antibody be higher during an infection

A

antigen higher at beginning

antibody higher at end

37
Q

What will the zone of equivalence show

A

high levels of immune complexes

38
Q

How will autoimmune disorders affect C3b

A

large amount of immune complexes which will exhaust the available C3b

once C3b is used. Will cause immune complexes to build up and become trapped

39
Q

What can occur if C3b is unavailable

A

immune complexes can become trapped and initiate an immune response

40
Q

What will occur after immune complexes become trapped in autoimmune disorders

A

initiate an immune response which will activate complement and cause a lot of inflammation

41
Q

What are examples of anaphylatoxins

A

C3a and C5a

42
Q

What is the action of anaphylatoxins

A

can bind directly to complement receptors on mast cells and basophils to cause degranulation without IgE

43
Q

What are the major results of anaphylatoxins

A

increase in vascular permeability and phagocytosis

44
Q

What type of infection is MAC critical in

A

Neisseria infections

45
Q

A patient has recurrent infections of meningitis, what complement is likely lacking

A

C5-C9 any of these

46
Q

What allows MAC to attack Neisseria

A

has lipooligosaccharide which is less bulky than LPS

47
Q

A patient presents with repeated infections of Neisseria meningitidis. What could be causing this

A

MAC deficiency

48
Q

What is the function of the C1 (C1 INH) inhibitor protein

A

inhibits C1r and C1s serine protease activity to turn off complement

49
Q

What is the function of decaying accelerating factor (DAF)

A

blocks formation of C3 convertase. Displaces Bb from C3b

50
Q

What pathway does C1 inhibitor affect

A

classical pathway, inhibits

51
Q

What is the distribution of DAF

A

leukocytes, epithelial cells, endothelial cells

52
Q

What is the function of CD59

A

blocks C9 binding and prevents formation of MAC

53
Q

What is the distribution of CD59

A

blood cells
endothelial cells
epithelial cells

54
Q

What proteins if inhibited would affect the classical pathway

A

C1q, C1r, C1s, C4 and C2

55
Q

What would be seen in a classical pathway deficiency

A

increased immune complex diseases and increased infections with pyogenic bacteria

56
Q

What pathway would a deficiency in C3 affect

A

both pathways. No complement can occur

57
Q

What would be seen in a C3 defienciency

A

recurrent bacterial infections and immune complex disease

58
Q

What pathway would a deficiency in C5-C9 affect

A

both pathways

59
Q

What would be seen in an individual with C5-C9 deficiency

A

recurrent meningococcal and gonococcal infections

60
Q

What will be seen in an individual with a deficiency in C1-INH

A

hereditary angioedema: overuse of C1, C4, and C2, edema at mucosal surfaces

61
Q

What is deficient in hereditary angioedema

A

C1-INH

62
Q

How can hereditary angioedema be treated

A

frozen plasma

LECOM Microbiology MS1 (22 decks)

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