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Overview of the Complement System

The document discusses the complement system, a crucial part of the immune response, detailing its history, components, and activation pathways including classical, lectin, and alternative pathways. It explains the roles of various proteins and factors involved in the complement cascade, leading to the formation of the Membrane Attack Complex (MAC) and the biological effects of complement activation. Additionally, it highlights regulatory mechanisms and potential deficiencies related to the complement system.

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0% found this document useful (0 votes)
3 views38 pages

Overview of the Complement System

The document discusses the complement system, a crucial part of the immune response, detailing its history, components, and activation pathways including classical, lectin, and alternative pathways. It explains the roles of various proteins and factors involved in the complement cascade, leading to the formation of the Membrane Attack Complex (MAC) and the biological effects of complement activation. Additionally, it highlights regulatory mechanisms and potential deficiencies related to the complement system.

Uploaded by

aozorarr160
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© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
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Chapter 4

Complement system

Tiana Milanda
Complement: History

o Discovered in 1894 by
Bordet
o It represents lytic
activity of fresh serum

o Its lytic activity is


destroyed when
heated at 56ºC for 30
min
Complement System
• Complement
– Consists of over 30 proteins
• Designated by C1(qrs), C2,
C3, C4, C5, C6, C7, C8, C9
• Factors B, D, H and I,
properdin (P)
• Mannose binding lectin (MBL),
MBL associated serine
proteases (MASP-1, MASP-2)
• C1 inhibitor (C1-INH, serpin),
C4-binding protein (C4-BP),
Decay Accelerating Factor
(DAF), Complement Receptor
1 (CR1), protein-S (vitronectin)
• Cascade of reactions
eventually
Pathways of complement
activation
CLASSICAL LECTIN ALTERNATIVE
PATHWAY PATHWAY PATHWAY

antibody antibody
dependent independent

Activation of C3 and
generation of C5 convertase

activation
of C5
LYTIC ATTACK
PATHWAY
Classsical
Pathway
• Classical pathway
– Initiated by antibody –
antigen reaction
Components of the Classical
Pathway

C1r
C1s
Ca++
C1q

C2 C3 C4

C1 complex

C1s is an enzyme and cleaves C4 and C2


Classical Pathway
Generation of C3-convertase

C4a C1r
C1s
Ca++

b
C4
C1q

Cleavage of C4 by C1s
produces C4a and C4b
Classical Pathway
Generation of C3-convertase

C4a C1r C2b


C1s
a C1s binds C2 and C2
Ca++ C2 is cleaved by C1s.
C1q C2b is released but
C2a remains bound
Mg++ to C4b on the
surface. C4b2a is C3
Convertase

C4b C2 a
Classical Pathway
Generation of C5-convertase

C4a C1r C2b C3a


C1s
Ca++ ________
C4b2a3b is C5 convertase; it
C1q leads into the Membrane Attack
Pathway
Mg++

C3 b
C4b C2 a
Classsical
Pathway
Lectin
Pathway
• Lectin pathway
– Released by
macrophages ingesting
microbes
– Lectins initiate
complement
Components of mannose-binding
lectin pathway

C4
MASP2
Pathogen

MBL C2 MASP1

• mannose binding lectin (MBL), MBL associated


serine proteases (MASP-1, MASP-2)
Mannose-binding lectin pathway

_____
C2b
C4b2a is C3 convertase; it will
C4a lead to the generation of C5
convertase

MASP1 C4b
C4
C2
MASP2 C2a
MBL C4b C2a

Binding to lectins cause autocatalytic activation


of MASPs, which then cleave C4 & C2
C5-convertase

C5-convertase of the
Classical and lectin
Pathways

C2a C3b
C4b
Lectin Pathway
Alternative
Pathway
• Alternative pathway
– Activated between
complement proteins and
microbe
Components of the
alternative pathway

fD

C3 fB
P

• fB = factors B, fD, H and I, properdin (P)


Spontaneous C3 activation

Generation of C3 convertase
D
H2O

B b
C3 C3 b

C3a
fB activate fD which then cut fB releasing
Ba, while Bb becomes an active protease
C3Bb complex has a very short half life
C3-activation
the amplification loop

If spontaneously-generated
C3b is not degraded

C3a C3b B b C3 b
C3-activation
the amplification loop

C3 b B b C3b

C3a C3b Bb
C3a
C3-activation
the amplification loop

Bb C3b
Bb C3b

C3a C3b Bb
C3a
C3a
Control of spontaneous
C3 activation via DAF

DAF prevents
the binding of C3b
B
factor B to C3b

DAF
CR1
Autologous cell membrane
Control of spontaneous
C3 activation via DAF

DAF dislodges
C3b-bound
B b B b C3b
factor Bb

DAF
CR1
Autologous cell membrane
C3b stabilization and
C5 activation
C3a
C3b finds an activator
(protector) membrane
This is stable C5 convertase of
P the alternative pathway
D

C3b
B b
C3 b
C5-convertase of the two
pathways

C5-convertase of the C5-convertase of the


Classical and lectin Alternative Pathway
Pathways

C3b Bb C3b
C2a C3b
C4b
Alternative Pathway
Pathways of complement
activation
CLASSICAL LECTIN ALTERNATIVE
PATHWAY PATHWAY PATHWAY

antibody antibody
dependent independent

Activation of C3 and
generation of C5 convertase

activation
of C5
LYTIC ATTACK
PATHWAY
Components of the lytic pathway

C7
C6
C5

C8
C
9
Lytic pathway
C5-activation

C5a

C5 b

C3b
C4b C2 a
Lytic pathway
assembly of the lytic complex

C5b first binds C6 and then C7


from the plasma. Membrane bound C6
C5b67 recruits C8 and C9 to form
the Membrane Attack Complex (MAC)
C7 C5 b
Lytic pathway:
insertion of lytic complex into cell membrane

C6

C8 C7 b
C5

C CC
99 9 C9
C
9 C
9
C
9 C C
9 9
Soluble Pattern Recognition Receptors-
Complement activation pathways
Biological effects of C5a
Biological Activities of
Classical Pathway Components
Component Biological Activity

C2b Prokinin; cleaved by plasmin to yield kinin, which


results in edema
C3a Anaphylotoxin; can activate basophils and mast
cells to degranulate resulting in increased vascular
permeability and contraction of smooth muscle cells,
which may lead to anaphylaxis
C3b Opsonin
Activation of phagocytic cells
C4a Anaphylotoxin

C4b Opsonin
34
Control of Classical Pathway
Components
Component Regulation

All C1-inhibitor (C1-INH); dissociates C1r and C1s from


C1q
C3a C3a-inactivator (C3a-INA; Carboxypeptidase B)

C3b Factors H and I; Factor H facilitates the degradation


of C3b by Factor I
C4a C3a-INH
C4b C4 binding protein (C4-BP) and Factor I; C4-BP
facilitates degradation of C4b by Factor I; C4-BP
also prevents the association of C2a with C4b thus
blocking formation of C3 convertase
35
C1-inhibitor deficiency:
hereditary angioedema
Complement System
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