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Host Defense Exam 1 > Complement > Flashcards

Complement Flashcards

1
Q

What are the general functions of complement?

A

recruit inflammatory cells (promote inflammation)

opsonize microbial pathogens and immune complexes (facilitate antigen clearance)

Kill microbial pathogens (via MAC)

Generate an inflammatory response

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2
Q

What are the three pathways of complement activation?

A

Classical pathway (Ag:Ab complexes)

Lectin pathway (Lectin binding to pathogen surfaces)

Alternative pathway (Pathogen surfaces)

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3
Q

How does the classical pathway work, and what components are involved?

A

C1q interacts with pathogen surface or with Ab attached to pathogen surface

C1q, C1r, C1s
C4
C2

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4
Q

How does the Lectin pathway work, and what components are involved?

A

Mannose binding lecting (MBL) and ficolins recognize and bind carbohydrates on pathogen surface

MBL/ficolin
C4
C2

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5
Q

How does the alternative pathway work, and what components are involved?

A

C3 undergoes hydrolysis to initiate deposition of C3 convertase on pathogen surface

Factor D
Factor B
Properdin
C3

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6
Q

What do all pathways eventually result in?

A

Generate a C3 convertase which cleaves C3 into membrane bound C3b and soluble C3a

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7
Q

What are the three results of complement activation, and what components are involved?

A

C3a and C5a recruit phagocytic cells to the site of infection and promote inflammation

Phagocytes with receptors for C3b phagocytose and kill the pathogen

MAC is formed which disrupts the cell membrane

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8
Q

When is classical complement pathway initiated?

A

After immune complex formation

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9
Q

How does the classical pathway recognize pathogen?

A

C1 binds to Ag:Ab complex

Ab binding to Ag leads to a conformational change in the Fc region of the Ab, allowing C1 to bind

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10
Q

What components make up C1?

A

C1qrs complex (C1q has globular heads and a tail)

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11
Q

what is required for activation of the C1qrs complex?

A

at least 2 Clq globular heads need to be bound to Ab, which means two Fc regions of Ab needs to be close on antigenic surface

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12
Q

What is different about IgM and IgG in regards to activating complement

A

As IgM is pentameric, only one IgM molecule bound to a given Ag is required to activate complement

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13
Q

What occurs after C1q binding?

A

C1r undergoes a conformational change, making it enzymatically active

C1r then cleaves C1s (a serine protease), which makes it enzymatically active as well

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14
Q

The activation of the Lectin pathway is similar to the classical pathway. What is the notable difference?

A

Instead of C1 binding to Ag:Ab, the Lectin pathway is initiated by a mannose binding lectin (MBL) or ficolins that bind to mannose and other complex carbs that are found on the surface of many pathogens (Candida albicans)

MBLs bind to Mannoses or Fucoses

Ficolins bind oligosaccharides containing acetylated sugars

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15
Q

What serine proteases are MBL and ficolin associated with?

A

MASP-1 and MASP-2, which are similar to C1r and C1s

These are activated when MBL/ficolins bind to Ag surfaces

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16
Q

Walk through the steps of complement complement sequence activation

A

Activated C1qrs (or MBL/ficolin:MASP-1/MASP-2) cleave C4, and the C4b fragment binds to the pathogenic cell surface. C4b binds C2

Once bound to C4b, C2 is cleaved by C1s(MASP-2) which forms the C4b2a complex, which is still bound to pathogenic surface

C4b2a is a C3 convertase, which can cleave C3 in C3b and C3a

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17
Q

What does C3b do?

A

C3b remains on pathogenic surfaces and is a powerful opsonin and enhances pathogenic phagocytosis

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18
Q

What is important about C3 convertases?

A

They are an important amplification in the complement cascade, as a single C3 convertase can cleave 1000 C3 molecules

19
Q

What is formed by the cleavage of C3 by C4b2a?

A

C4b2a3b, a C5 convertase

20
Q

What does C5 convertase do?

A

C5 convertase cleaves C5 into C5a and C5b

C5a is a powerful inflammatory mediator

C5b acts with other complement components to form the MAC

21
Q

What do C3a and C5a do?

A

They remain soluble and produce local inflammatory effects

22
Q

Walk through the process of MAC formation

A

C5b binds C6 and C7

The C5b67 complex binds to pathogen surface via C7

C5b67 binds C8, which inserts into the membrane

1-16 C9 molecules bind to the complex, polymerize, and form a pore which lyses the pathogen

23
Q

What does the alternative pathway depend upon?

A

The slow hydrolysis of C3, which spontaneously occurs in plasma

24
Q

What does hydrolyzed C3 do?

A

Hydrolyzed C3 can bind Factor B, which can then be cleaved by factor D into Ba and Bb

The resulting C3b(H2O)Bb complex is a C3 convertase that can cleave C3 into C3a and C3b

C3b is rapidly degraded unless it binds to a pathogenic surface

25
Q

What else does factor B bind to?

A

factor B can bind non-covalently to C3b on a cell surface and be cleaved by factor D into Bb and Ba, forming the C3 convertase C3bBb

26
Q

What stabilizes the C3bBb complex?

A

properdin (Factor P)

27
Q

How does the alternative pathway activate C5?

A

C3bBb binds another molecule of C3b, forming the C5 convertase C3bBbC3b

28
Q

What is the biological consequence of complement activation?

A

cell lysis (gram negative) and viral neutralization

29
Q

How does opsonization work?

A

Phagocytic leukocytes carry receptors to C3b (CR1)

Ag coating by C3b will enhance the phagocytosis of the cell by the phagocytes

30
Q

How does C5a also participate in phagocytosis?

A

It encourages phagocytes to take up C3b coated Ag

31
Q

How do RBCs participate in the clearance of immune complexes?

A

RBCs have the receptor for C3b, CR1. Therefore, RBCs will bind and carry immune complexes through the circulation to the spleen and liver, where the coated complexes are stripped off by resident phagocytes

32
Q

How do the soluble components of complement stimulate inflammation?

A

C5a is a chemoattractant for basophils, monocytes, eosinophils, and neutrophils

C3a, C4a, and C5a are anaphylatoxins - they stimulate basophils and mast cells to release histamine which results in increased vascular permeability

33
Q

What inhibits C1?

A

C1 inhibitor (C1INH) - inhibits C1 by dissociating C1r and C1s from the immune complex

34
Q

what inhibits the C3 convertase?

A 
Decay accelerating factor (DAF)
C4 binding protein (C4BP)
Complement receptor 1 (CR1)
Membrane cofactor protein (MCP)
Factor I (I)
35
Q

What inhibits C5 convertase?

A 
Factor I (I)
Factor H (H)
Complement receptor 1 (CR1)
36
Q

What prevents assembly of MAC?

A

CD59

37
Q

What do deficiencies in the classical pathway result in, and what components are involved?

A

C1, C2, C4 deficiencies can result in immune-complex disease

38
Q

What do deficiencies in the lectin pathway result in, and what components are involved?

A

MBL, MASP1, MASP2, C2, C4 deficiencies can result in bacterial infection, mainly in childhood

39
Q

What do deficiencies in the alternative pathway result in, and what components are involved?

A

Factor P, Factor D deficiencies can result in pyogenic bacteria and Neisseria spp. but no immune complex disease

40
Q

What do deficiencies in C3b deposition result in, and what components are involved?

A

C3 deficiencies can result in infection by pyogenic bacteria and Neisseria spp., sometimes immune complex disease

41
Q

What do deficiencies in MAC formation result in, and what components are involved?

A

C5, C6, C7, C8, C9 deficiencies lead to infection with Neisseria spp. only

42
Q

What results in failure to regulate complement?

A

Hereditary Angioneurotic Edema: C1INH deficiency - failure to regulate C1 resulting in fluid accumulation and epiglottal swelling

Paroxysmal Nocturnal Hemoglobinuria: failure of C59 function - lack of complement regulation leads to RBC lysis

43
Q

What happens if immune complexes are not cleared?

A

It can result in renal disease (thus CR1 is really important)

Host Defense Exam 1 (13 decks)

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