immediate innate immunity (exam 2) Flashcards
defense is based on where
pathogens reside
defense mechanisms against pathogens are
on intact epithelial surfaces
in tissues underneath
types of infections
extracellular
intracellular
immediate innate immune response
0-4 hours after infection
performed effector molecules and resident effector cells in infected tissue
performed effector molecules include
complement
defensins
pentraxins
resident effector cells in infected tissue include
macrophages
dendritic cells
major consequence of innate immunity
inflammation
complement
one of the first weapons
soluble proteins made by the liver
made up of over 30 proteins
complement is present in
the blood, lymph, and extracellular fluids
how does complement make the pathogen more easily phagocytosed?
it coats the surface of bacteria/extracellular viruses
most important component of compliment
C3
cleavage of C3a (small) and C3b
in the innate immune, infection triggers
complement activation cascade
3 pathways of complement activation
alternative
lectin
classical
all pathways of complement activation lead to
C3 cleavage
deposition of C3b
recruitment of similar effector mechanisms to destroy pathogens
types of C3 convertases
iC3Bb (soluble C3 convertase)
C3bBb (alternative C3 convertase)
iC3Bb
initial hydrolysis of C3 is catalyzed by environment near bacterial surface
Complement control proteins
plasma proteins
membrane proteins
regulation of complement activation
combined effect of promoting and regulating C3 activation
deposit C3b on pathogen surface, not human cells
self from nonself
first effector cells encountered
macrophages
macrophages _______ many pathogens using ________
phagocytose
MO receptors
examples of complement receptors that bind C3b
CR1, CR2, CR3 and CR4
opsonization
coating of pathogen with protein that facilitates phagocytosis
C5
similar to C3
initiates formation of membrane attack complex which makes holes in cell membranes
C3b2Bb
alternative C5 convertase –> C5a and C5b
C6, C7
recruited by C5
C8
binds C5b and exposes hydrophobic site
C9
forms transmembrane holes
deficiency in C5-C9
more susceptibility to infections
not uncommon
inherited deficiency in C3
more severe
frequent bouts of infection
Regulation of terminal complement proteins
soluble proteins and membrane proteins
(dec activity of making holes in the membrane)
paroxysmal nocturnal hemoglobinuria
complement mediated lysis of RBC
attacking self
anaphylatoxins
C3a and C5a
increase inflammation
facilitates plasma protein and cell transport to infection
in anaphylatoxins are systemic, they can induce
anaphylactic shock
anaphylatoxins increase inflammation by
binding receptors of several cells
attract neutrophils and monocytes
trigger release of histamine and other substances
other plasma proteins that inhibit infection
coagulation system
kinin system
protease inhibitors
a2-macroglobulins
inhibit proteases that break down tissues
kinin system
increase vasodilation
triggered by tissue damage
coagulation system
clots
closes off where pathogen is going
defensins
antimicrobial peptides
amphipathic
penetrate microbial membranes
denature microbial toxins
defensins are for
why?
human cell protection
they produce in inactive form and function poorly in physiological conditions
defensins are active in
tears, sweat, phagosome, etc.
defensins are found in ______ and _______
neutrophils
paneth cells
defensins differ in
amino acid sequence
specificities for microbes
area protected
Pentraxins
plasma proteins that bind microbes and deliver them to phagocytes
function similar to antibodies
