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SBB > Complement > Flashcards

Complement Flashcards

1
Q

What are the functions of Complement?

A 
Bind and clear cells
Opsonization
Inflammation C5a and C3a
Lysis of foreign cells
Enhance antibody response
Maintain B cell tolerance
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2
Q

What is required for Complement activation?

A

Calcium us required. EDTA chelates Ca so complement activity only found in serum

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3
Q

Properties of Complement system

A

Lytic properties are destroyed by heating at 56C for 30
C’ proteins are not immunoglobulins = they don’t increase concentration when immunized
Circulate in the inactive form = zymogen
C’ is not species specific

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4
Q

What chromosome are C2 and C4 located on?

A

Chromosome 6

MHC Class III

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5
Q

What are opsonins?

A

Not necessarily complement proteins
Can be antibodies or CRP
Tag pathogen for phagocytosis

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6
Q

How is the classical pathway activated?

A

IgG/IgM
DNA or Chormatin
Free Hgb (sickle cell Hyper hemolysis)
Gram negative bacteria

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7
Q

How is the alternative pathway activated?

A

Endotoxins, IgA, and Immune complexes
Activated by cell surface polysaccharides
Does not require antibody
C3 is hydrolyzed by H2O
C3b binds to factor B
Factor D cleaves B = C3bBb + Properdin = C3 convertase

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8
Q

How is the mannose binding lectin pathway activated?

A

Mannose on bacterial cell walls
Antibody independent - MBL is antibody like
MLB is similiar to C1
Mannose is found on HIV, Influenza, Salmonella, Strept, and candida
MLB is an acute phase protein produced during inflammation

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9
Q

What is the recognition unit in the classical pathway?

A

AB/AG complexes bind Fc portion to C1q to activate
2 IgG constant heavy chains (Fc) bind to C1 or 1 IgM
Only IgG1 and IgG3 can activate complement
C1 complex = C1q, C1r, C1s plus Ca+

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10
Q

What is C1 inhibitor deficiency?

A

C1 inhibitor binds to C1rs and dissociates C1q
C4 will not bind
Deficiency in inhibitor = Hereditary angiodema
uncontrolled C’ antivation

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11
Q

What is the activation unit in the classical pathway?

A 
C1s cleaves C4 and C2
C4b binds to cell
C2a binds to C4b = C3 convertase
C3 convertase = C3a + C3b
C3b binds to cell
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12
Q

What happens with C3b is bound to cell surface?

A
  1. C3b can be inactivated by C3 inactivator (Factor I or H)
  2. Macrophages bind complement and phagocytise
  3. C3b binds to C4b2a = C5 = MAC formation
  4. RBC’s may be temporary sequestered
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13
Q

How is MAC formed?

A 
C3 convertase splites C3>C3b and C3a
C3b binds to cell membrane
C4b2a binds to C3b > C5 convertase 
C5 converatase = C5a and C5b
C5b binds to cell. C6, C7, C8, C9 bind to C5b.
Punch hole in cell = Cell lysis
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14
Q

What is the function of C3a and C5a?

A

Anaphylatoxins. Histamine is released from basophils and mast cells. Shock results when systemic preability from vasodilation > hypotension > organ failure > cardiac arrest > death
C5a is also chemotaxic

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15
Q

What is function of C3b?

A

Opsonin

Promotes phagocytosis

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16
Q

What is C3d?

A

C3d is formed from C3b by factor H
C3d is more stable
Complement control cells are C3d

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17
Q

What is C4d?

A

C4b is degraded into C4d by Factor H
C4d is Chido/Rogers antigens
C4d covalently attaches to RBC membrane.
Ch/Rg is found in plasma

18
Q

What gene encodes for Rogers?

A

C4A gene
Lack of C4A results in a much greater susceptibility to systemic lupus erythromatosis = Rg-
Binds IC and has stronger affinity for CR1

19
Q

What gene encodes for Chido?

A

C4B gene

Lack of C4B results in increased susceptibility to bacterial meningitis in children

20
Q

What is the innocent bystander effect?

A

Soluble phase complement will react with any cell including host cells
Once activated it will attach to any cell
C5-8, once formed, C9 binds spontaneously

21
Q

What is the function of Complement Receptor 1?

A

CR1 stimulates phagocytosis + Clears immune complexes
Binds C3b and C4b
located on Macro, segs, and dendritic cells
CR1 is on RBC’s and PLT’s and transport IC to the liver
Knops antigen

22
Q

What is the function of Complement Receptor 2?

A

Located on B cells and dendritic cells
Part of B cell co-receptor
Ebstein Barr virus receptor

23
Q

What is the function of Complement Receptor 3?

A

Located on Myeloid, Macro’s, and NK cells

Phagocytosis

24
Q

How is C’ regulated?

A

Activated components are short lived
Fragments don’t reattach
Control proteins dissociate C3 and C5 convertase

25
Q

What is DAF?

A

Decay accelerating factor = CD55 = Cromer antigen
Inhibits production of C3 convertase
Protects self cells from complement
Lack of DAF = PNH = complement mediated hemolysis
- Acquired mutation caused by lack of GPI so DAF can’t bind to cell

26
Q

What is C1 esterase inhibitor?

A

C1INH
Inhibits activation phase
Combines with C1q

27
Q

What is Factor H?

A

Regulates Alternative pathway

Dissociated C3bBb from cell = NO C3 convertase

28
Q

What is Factor I?

A

C3 inhibitor

Cofactor for factor H

29
Q

What is C4BP?

A

C4 binding protein

Bind to C4b = stops C3 Convertase from forming

30
Q

What antigens are located on CR1?

A

Knopps antigens

Kna, McCa, Sia, Yka

31
Q

What is CD59?

A

Inhibits MAC by binding C8

MAC Control by MIRL (CD59, HRF)

32
Q

What causes Hereditary Angioderma?

A

C1 esterase inhibitor deficiency
Uncontrolled action of C1 on C4 and C2 > large amounts of vasoactive peptides formed > increased vascular preablility > Swelling of the skin, GI, and respiratory track

33
Q

What is C3 nephritic factor?

A

Autoantibody found in patients with mesangioglomerulonephritis.
Binds to C3bBb and stablizes > Complement activation > MAC

34
Q

What causes CR1 deficiency?

A

CR1 on RBC’s and PLT’s transport IC to liver. Every time CR1 is lost. WAIHA or SLE may have decreased CR1

35
Q

What are signs of C3 receptor deficiency?

A

Poor neutrophil infiltration
Infants will have delayed separation of umbilical cord, recurring ulcerating infections, abnormal paper thin scar formation

36
Q

What is the Helgeson phenotype?

A

Low numbers of CR1 and may antigen type as negative

XM compatible with older units because CR1 is shed in storage

37
Q

What is Inab phenotype?

A

No DAF on RBC

38
Q

What antibodies can bind C’?

A

IgG1 ++, IgG3 +++, and IgM ++++
IgGw weakly binds C’ - Can also activate alternative
IgA, IgE, IgD can’t bind C’
(IgA can activate alternative)

39
Q

Where are Complement proteins formed?

A

In macrophages and parenchymal cells in the liver

40
Q

What are Characteristics of Ch/Rg antibody?

A

Formed in multiply transfused patients

Can type as Chido or Rodgers positive but make an antibody because it is polymophic

41
Q

What cells are CR1 and CR3 found on?

A

Macrophages

42
Q

Susceptibility to complement-mediated lysis is associated with which blood group antigens?

A

Cromer = DAF

SBB (37 decks)

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