772
UNIT 4
Maintenance of the Body
21
Te
alternative pathway
is triggered when spontaneously
activated C3 and other complement factors interact on the
surface of microorganisms. Tese microorganisms lack the
complement activation inhibitors our own cells have.
Like the blood clotting cascade, complement activation by
any of these pathways involves a cascade in which proteins are
activated in an orderly sequence—each step catalyzing the next.
Te three pathways converge at C3, which cleaves into C3a and
C3b. Tis event initiates a common terminal pathway that en-
hances inflammation, promotes phagocytosis, and can cause
cell lysis.
Cell lysis begins when C3b binds to the target cell’s sur-
face and triggers the insertion of a group of complement pro-
teins called
MAC (membrane attack complex)
into the cell’s
Figure 21.6
outlines the three pathways by which comple-
ment can be activated.
Te
classical pathway
involves
antibodies
, water-soluble pro-
tein molecules that the adaptive immune system produces to
fight off foreign invaders. When antibodies bind to patho-
gens, they can also bind complement components. Tis dou-
ble binding, called
complement fixation
, is the first step in this
complement activation pathway. (We describe this in more
detail on p. 782.)
Te
lectin pathway
involves
lectins
, water-soluble protein
molecules that the innate immune system produces to rec-
ognize foreign invaders. When lectins bind specific sugars
on the surface of microorganisms, they can then bind and
activate complement.
Activated spontaneously. Lack of
inhibitors on microorganism’s
surface allows process to proceed
Classical pathway
Alternative pathway
Activated by
lectins
binding to
specific sugars on
microorganism’s surface
Lectin pathway
Enhances inflammation:
Opsonization:
Complement
proteins
(C5b–C9)
Pore
Membrane
of target cell
C3
C3a
C5a
C3b
C3b
C5b
C6
C7
C8
C9
MAC
Coats pathogen surfaces,
which enhances
phagocytosis
Stimulates histamine
release, increases blood
vessel permeability,
attracts phagocytes by
chemotaxis, etc.
Activated by
antibodies
coating
target cell
Together with other complement
proteins and factors
MACs form from activated
complement components (C5b
and C6–C9) that insert into the
target cell membrane, creating
pores that can lyse the target cell.
Figure 21.6
Complement activation.
All three pathways that activate complement
converge at C3. C3 splits into two active pieces: C3a and C3b, which enhance inflammation
and act as opsonins. In certain target cells (mostly bacteria), C3b also activates other
complement proteins that can form a membrane attack complex (MAC).
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