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Chapter 13

Chapter 13 discusses the effector mechanisms of humoral immunity, focusing on the structure and function of Fcγ receptors and the complement activation pathways. It details the alternative, classical, and lectin pathways of complement activation, highlighting the roles of various components like C3b and C5 convertases. The chapter concludes with the late steps of complement activation, including the formation of the membrane attack complex (MAC) that leads to cell lysis.

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3 views27 pages

Chapter 13

Chapter 13 discusses the effector mechanisms of humoral immunity, focusing on the structure and function of Fcγ receptors and the complement activation pathways. It details the alternative, classical, and lectin pathways of complement activation, highlighting the roles of various components like C3b and C5 convertases. The chapter concludes with the late steps of complement activation, including the formation of the membrane attack complex (MAC) that leads to cell lysis.

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suhanis.bits
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd

Chapter 13

Effector Mechanisms of Humoral Immunity


FIGURE 13.3 Subunit composition of Fcγ
receptors. Schematic showing human Fcγ
receptors with Fc-binding α chains and
signaling subunits. FcγRIIIB is GPI-
anchored and lacks signaling function,
while FcγRIIA and FcγRIIC are low-affinity
activating receptors with distinct expression
patterns. Although FcγRIIA/C and FcγRIIB
share the CD32 designation, they are
structurally and functionally different. The
neonatal Fc receptor (FcRn) resembles
MHC class I structurally but lacks a peptide-
binding cleft.
FIGURE 13.6 Early steps of
complement activation.
The alternative pathway is
triggered by C3b binding to
microbial surfaces, the classical
pathway by C1 binding to
antigen-antibody complexes, and
the lectin pathway by plasma
lectin binding to microbes.
Generated C3b attaches to the
surface or antibody and forms
part of the C5 convertase,
initiating the late steps of
complement activation, which
are common to all three
pathways.
FIGURE 13.7 Alternative pathway of
complement activation.
Spontaneous C3 hydrolysis generates
C3*, which deposits on microbial
surfaces, binds Factor B, and forms the
C3 convertase (C3bBb). This enzyme
produces more C3b, amplifying the
response and forming the C5 convertase
(C3bBbC3b), which cleaves C5 to C5b,
initiating the late steps of complement
activation.
FIGURE 13.9 The classical pathway
of complement [Link]-
antibody complexes that activate the
classical pathway may be soluble,
fixed on the surface of cells (as
shown), or deposited on extracellular
matrices. The classical pathway is
initiated by the binding of C1 to
antigen-complexed antibody
molecules, which leads to the
production of C3 and C5 convertases
attached to the surfaces where the
antibody was deposited. The C5
convertase cleaves C5 to begin the
late steps of complement activation.
FIGURE 13.12 Late steps of complement
activation and formation of the membrane
attack [Link] cell-associated C5
convertase cleaves C5 and generates C5b,
becomes bound to the convertase. C5b binds
C6 and C7 sequentially, and the C5b-7 complex
inserts into the plasma membrane, followed by
addition of C8 to the complex, which forms
unstable pores. The C5b-8 complex can form a
pore with C9, and C9 can also be induced to
homo-oligomerize by the C5b-8 complex. As
many as 15 C9 molecules may polymerize to
form the membrane attack complex (MAC),
which creates pores in the membrane and
induces cell lysis. C5a released on proteolysis
of C5 stimulates inflammation.

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