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IMM Exam 1 > Complement > Flashcards

Complement Flashcards

1
Q

complement important in defense against which kind of organisms?

A
  • pyogenic
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2
Q

roles of complement

A
  • promotes inflammatory response
  • eliminates pathogens
  • enhances immune response
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3
Q

complement and immune complex diseases

A
  • component in both prevention and pathogenesis of immune complex diseases
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4
Q

functions of complement

A
  • opsonization
  • inflammation
  • lysis
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5
Q

opsonization

A
  • attaches immune cells or antibodies to invading organism

- helps with phagocytosis by PMN/macrophages

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6
Q

inflammation

A
  • induces acute inflammation to dilate blood vessels
  • activates mast cells/basophils
  • recruits inflammatory phagocytic cells to eat invading organisms
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7
Q

lysis

A
  • generates a group of proteins to form membrane attack complex
  • penetrate invading cell’s wall to induce lysis
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8
Q

complement timing in immune response

A
  • one of the earliest immune responses
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9
Q

alternate complement pathway

A
  • C3 -> C3b
  • C3b -> C3bBb (C3 convertase) converts for C3 to C3b
  • C3bBb3b (C5 convertase) converts C5 to C5b
  • C5b interacts with C6-C9 to form membrane attack complex
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10
Q

lectin pathway

A
  • C1-like complex converts C4 to C4b
  • C4b interacts with C2b from classical pathway to form C4b2b (C3 convertase)
  • Converts C3 to C3b
  • forms C4b2b3b (C5 convertase) converts C5 to C5b
  • C5b interacts with C6-C9 to form membrane attack complex
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11
Q

classical pathway

A
  • C1 present
  • converts C2 to C2b
  • C2b interacts with C4b from lectin pathway to form C4b2b (C3 convertase)
  • Converts C3 to C3b
  • forms C4b2b3b (C5 convertase) converts C5 to C5b
  • C5b interacts with C6-C9 to form membrane attack complex
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12
Q

starting points of alternative pathway

what branch of immune system

A
  • C3
  • factor B, D
  • properdin
  • innate immune system
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13
Q

starting points of lectin pathway

what branch of immune system

A
  • plasma-derived mannose-binding lectin
  • MBL
  • innate immune system
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14
Q

starting points of classical pathway

what branch of immune system

A
  • C1qrs
  • C2
  • C4
  • adaptive immune system
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15
Q

trigger start of alternative pathway

A
  • complement components bind on microbial surfaces and cannot be turned off
  • SPONTANEOUS
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16
Q

trigger start of lectin pathway

A
  • MBP normally exists in circulation
  • MBP binds to mannose on bacterial surface
  • produces enzyme to cleave C4 into C4b and C2 into C2b
17
Q

trigger start of classical pathway

A
  • interaction of Fc portion of antibody
    • IgM
    • IgG1, IgG2, IgG3
  • c reactive protein with C1q

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18
Q

why can complement components not be turned off by microbes?

A
  • their regulatory proteins only exist on host cells, not microbial surfaces
19
Q

common goal of all three pathways

A
  • make C3b

- deposit C3b on clusters on the target

20
Q

which acts as an opsonin?

How does it act as an opsonin?

A
  • C3b
  • C3b recognized by complement receptor type 1 on phagocyte
  • microbes phagocytosed
21
Q

which are the anaphylaxotoxins

A
  • C3a, C4a, C5a

think A causes Anaphylaxis

22
Q

which are the chemoattractants?

A
  • C3a, C5a
23
Q

what do the anaphylatoxins do?

A
  • increases vascular permeability to enhance movement of leukocytes and plasma proteins into tissues
24
Q

do you chemoattractants do?

A
  • attract neutrophils and monocytes for destruction of pathogen
25
Q

how does the membrane attack complex kill cells?

A
  • creates perforations in cellular membranes

- induces osmotic lysis of cells

26
Q

what is the membrane attack complex effective against?

A
  • microbes with thin cell walls (gram negatives)

- Neisseria species

27
Q

decay accelerating factor (DAF) function

A
  • down regulates C3 convertase

- displaces Bb from C3b

28
Q

DAF deficiency

A
  • also known as CD55 deficiency
  • uncontrolled complement activation that leads to RBC lysis
  • leads to paroxysmal nocturnal hemoglobinuria
29
Q

C1 inhibitor

A
  • protease inhibitor
  • down regulates C1r and C1s activation in classical pathway
  • prevents complement activation on self cells
30
Q

C1 esterase inhibitor deficiency

A
  • uncontrolled C1 activation
  • leads to excessive vasoactive peptides being generated
  • leads to hereditary angioedma
31
Q

why C1 inhibitor deficiency can lead to hereditary angioedema

A
  • unrelated activation of kallikrein to bradykinin
32
Q

role of bradykinin

A
  • vasodilation and increases vascular permeability

- ergo edema

33
Q

what characterizes C1 esterase inhibitor deficiency

A
  • low C4 levels

- high bradykinin

34
Q

C3 deficiency

A
  • risk of encapsulated bacterial infection

- recurrent pyogenic infections

35
Q

C5b-C9 deficiencies

A
  • increased susceptibility to Neisseria infections

- severe pyogenesis and sepsis in infants

36
Q

C1, C2, C4 deficiency

A
  • associated with immune complex disorders

- especially SLE

IMM Exam 1 (20 decks)

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