L02 - Innate Immune Defences 1 Flashcards
what is innate immunity
time frames of it occuring?
what are the characteristics of innate immunity
innate barriers to infection
what are the three main types. and examples.
physical
soluable - complement and defensins and collectins
induced - innate immune cells, PRRs and interferon
what happens when there is tissue damage
soluable innate immune molecules
what are there out there,
and what do they (briefly) do???
lysosome
antimicrobial peptides
collectins, ficolins and pentraxins
complement compnonents
lysosome
what is it what does it do
what is secreted by??
what is most effective against
what does it do to a molecular level??
phago’s, also paneth cells by SI
gram positive bacteria
antimicrobial peptides
what are the different types of these. what are they effective against
what do they cover and where are they found
what secreted by
what do they do, what do they attack and what else do they do
histatins, defensins, cathelicidins
defensins
what are the two classes of them
what is their rough molecular structure and properties
what do they do
amphipathic peptides
COLLECTINS, FICOLINS AND PENTRAXINS
— what are their actions??? what are they?? what do they act as??? what does this lead to??
collectins - what is their structure what does it do
ficolins - what do they do
pentraxins - what are they where are they found
what is CRP
COMPLEMENT SYSTEM
what is it, what does it do. what is it produced by
how do the components travel in the blood
what property do some of them have
what happens when they are activated (on a molecular level) — exceptions
most made by liver but also by monocytes/macrophages and epithelial cells of intestine and urinary tract
c2a
COMPLEMENT SYSTEM
what are the diff cascades
what are the two main effects which the complement components mediate?? what are the activities of these effects.
classical pathway
what is it initiated by
what is the structure of the thing that activates it
what must this do
what are most effective at activating complemet. what about execptions
how is it amplified?????????
–
c1 - C1q, C1r, C1s. ———C1q dominates
IgM (not in serum) also IgG 1,3,2
classical pathway
how is it amplified
LECTIN PATHWAY
what is it activated by??? (and not)
what happens molecularly??
what does it effect
what is it similar to
what is formed once the activation thing has bound??? what does this do????
ficolins and MBL —- INDEPENDANT from antibody
ALTERNATIVE PATHWAY
how does this happen. — what are the molecular steps what cleaves and bonds and why
c3 – hydol c3a and c3b
c3b binds to cell mem and factor B – suceltable to cleaveage by factor D to Bb.
C3bBb binds to protein properdin
then this can hydrolyse more c3, creating morr C3b, amplifying the signal
