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Innate Immune System Concept Map

cox enzyme
(cyclooxygenase)
Lipooxygenase
CXCLB, a chemokine,
cacuse a conformational
change in the
ICAM/integrin adhesion,
strengthening it
Neutrophils emigrate
frist and monocytes
move late using
a similar meachanism
(as'VCAM' in monocytes and
VLA -4 in neutrophils
take 24hrs to be expressed)
Lymphocytes, esoinophils
and plasma cells may
follow later
Activation
of
Intergrins
'Diapedes'
neutrophils squeeze
between neighbouring
endothelial cells and
cross the basement
membrane by
secreting proteases to
break it down
Bind to
integrins
(e.g. LFA-1)
on the
neutrophils
Expression of
immunoglobin-like
molecules (which
belong to the
superfamily e.g.
ICAM-1) by
endothelial cells
Production of
inflammatory
Cytokines
E.g, IL-1 and TNF and
CXCL8
Over expression
of P and
E-selectin by
endothelial cells
Bind to
sialylated
glycoprotein
lgands on
neutrophils
Rolling of
neutrophils
along
endothelium due
to disrupted
weak
interactions
Other effects of
cytokines
(See inflammatory
cytokines flow
chart)
Complement
system
Complement
system
Complement
system
movement of
proteins and
leukocytes from
blood into tissue
fluid space
Fibrinogen
converted to
fibrin by
thorombin
Forms insoluble
strands which
produce a web to
contain infection
and inflammation
Fromation of
inflammatory
Exudate
Swelling
('Tumor')
Pain ('Dolor')
Monocytes
mature to from
marcrophages
'Chemotaxis'
All leukocytes are
stimulated to migrate
towards the infected area
along CXCL8 gradients
increased
vascular
permeability
Shrinking of
endothelial
cells
Histamine
blood vessel
endothelium
Overxpression
of P-selectin by
endothelial cells
Heat
( 'Calor')
Redness
('Rubor')
vasodilation
Histamine on
smooth muscle
cells on
vascular walls
PAIN
('Dolor')
Histamine
receptors on
nerve ending
Mast cells
degranulate and
secretion preformed
histamine
Inflammatory exudate
Effects of histamine
Recruitment of leukocytes using
cytokines and chemokines
Change in
gene
expression
Signals
sent to
nucleus of
sentinel cell
Sentinel cell
activation
PAMP
recognised
by PRR on
sentinel cell
(usually
resident
macrophage)
Pathogens
express
PAMP
Sentinel Cells
Secrete
Type ll
interferon,
IFNY
Activate Natural
killer (NK)_ cells
Release
granules
containing
perforin
and aporptosis
inducing
granzymes
Perforin
perforates
membrane
of target
cell and
granzyme
s enter,
inducing
apoptosis
NK cells
'Recognition
of missing
self' by NK
cells
Down regulation
of Major
Histocomptibiliy
Complex Class l
molecules
Interfere
with viral
replication
Infected cell
Secrete Type
I INterferons
(e.g. IFN a &
IFNB)
'Antibody Dependent
Cytotoxicity' (ADCC)
Antibodies detected
via Fc Receptors on
NK cells
1-2 hrs
Other stress
Cell membrane
injury
Activation of
platelet
activating
factor found in
the lipid bilayer
Arachidonic
acids in
phospholipid
bilayer
converted
Prostaglandins
Leukotriene
Prostacyclim
Thromboxane
Vasodilation
Platelet
aggreation
Pathogen
enter
Lipid inflammatory mediators
INNATE IMMUNE SYSTEM
28
author vip Blackwood
This concept map of the innate immune system depicts pathogen exposure. By adulthood, most people have been exposed to various pathogens and developed stronger immunity. Once an antibody is produced, the body stores a copy of it so that if the same antigen appears again, the body can deal with it more quickly. Some diseases, such as measles, can be fatal if untreated, so experts advise vaccination. A person who has received the measles vaccine is unlikely to contract the disease. It is also uncommon for an unvaccinated person to contract measles again. The body stores a measles antibody in both cases. As shown in this image, the antibody is prepared to destroy the virus the next time it appears.
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