lecture 10 Flashcards
(26 cards)
what is the first line of defenses of innate immunity?
provided by?
physical & chemical barriers that prevent infection
epithelial cell layers, mucosal tissues (GI, respiratory, urogenital), glandular (salivary and mammary)
what is the second line of defenses on innate immunity do?
-recognize pathogen components & trigger variety of cellular responses
-pathogen recognition by receptors activates some cells to phagtocytose & degrade pathogen
what is inflammation?
inane immune kills pathogen & produces cytokines & chemokines—-> which recruit cells, molecules & fluid to site of infection
two major comments of innate immunity?
soluble mediators & cellular mediators
what are soluble mediators?
cytokines, antimicrobial peptides, complement
what are cellular mediators?
NK cells and PAMP-PRR interactions
what are cytokines?
produced by?
what can cytokines be produced into?
what are chemokiness?
proteins that stimulate or inhibit differentiation, proliferation & function
immune & non immune cells, one may produce many
interleukins: act on leukocytes
interferons (IFNs): prevent viral infection
—family of cytokines that selectively induce chemotaxis & activate leukocytes
what is the complement system?
activation— initiators bind to pathogens (classical, lectin, alternative)
proteolytic cascade—–makes proteins of complement cascade C3 and C5
outcomes—
opsonization–coating pathogen w antibodies or complement proteins
,inflammation
cell lysis by MAC
what are cell mediators?
cells?
receptors?
phagocytes & NK
PAMPS on microbes recognized by PRRs on host cells
PAMP-PRR makes inflammation
sensor cells express ______ for an intial discrimination between self and non self
pattern recognitions
-neturophils & macrophages
what is the order cells during infection?
iFN and iL —> NK mediated killing–> T cell killing
5 characteristics of NK?
What cytoxins do they release?
lyse cells lacking MHC class 1
secretes cytokines—IFN & perforin dependent cytolysis
Perforin & granzyme—- perforin forms a pore and granzyme cleaves proteins in cells
controlled by activating & inhibitory receptors
what causes inhibitions & NK activation?
If there is no self MHC class 1— activation receptors will be turned on, which will result in target cell killing
If there is self MHC class 1— inhibitor response will be activated
what is PAMPS?
where can they be?
expressed only in microbes & recognized by innate immune cells –NOT IN HUMAN CELLS
–repeating structural motifs common to many microbes
surface pattern or inside
what are PRR?
part of what type of immune system?
associate with?
major subtypes?
receipts on host cells , recognize PAMPS
-innate
subcellular compartments – membranes, cytosol
TLR, NLR, RLR, cGAS
what are ex of PAMPS in bacteria, viruses & fungi?
bacteria surface: cell wall, flagella
intra: genome—»unmeth CPg
viruses surface: cell surface proteins
intracellular : ds RNA and ssRNA
fungi: only cell wall (surface)
function of TLR in innate immune repose?
TLR binds PAMPs—> pathway activated depends on TLR & adaptor protein (MyD88 or TRIF) that binds to TLR cytoplasmic TIR domain
signalling activated NFkb, IRFs and TF like AP1– downstream of MAPK pw
turns genes on or off
what are the type of IFN during covid infection, low & high viral load?
low— early IFN response–> rapid viral clearance
high— delayed—> viral persists–> severe
TLR, which recognize nucleotides?
cGAS do?
TLR: bind PAMPS to activated signal pathways
intracellular 3,7,8,9
extraceullar recog cell wall or flagella
cGAS: recognize cytosolic DNA from virus or bacteria
what is NLR and RLR?
NLR: intracellular sensors of fragments of bacterial cell walls
RLR: RNA helices that act as cytosolic PRR that recognize dsRNA
which TLR members recognize nucleic acids in edosomes ? what is the effector cytokine produced by these TLRs?
TLR 3,7,8,9
type 1 IFN (Alpha and beta) that has antiviral activities
which TLR are expressed on cell surface? what are main cytokines produced by them?
TLR1,2,4,5,6
activate IL1,6, and TNF a–> for inflammation
how is local inflammation controlled ?
-tissue damage via vasodilation–> increasing flow & cap permeability
-increase cap permeability leading to leakage of fluid into tissues
-influx of neuropils & other phagocytes from blood into tissues
-phagocytes & antibacterial destroy bacteria
what are the 1-3 steps of innate immune response?
–enter of pathogen via lesion in epithelial barrier–> attack by effector molecules & cells that make inflammation
–expression of antimicrobial and proinflammatroy molecules induced by:
extracellular pathogens recognized by plasma membrane OR PRR
intracellular pathogens in infected cells recognized by cytsolic PRR
— extracellular pathogens with surface components recognize by certain PRR & cleared by phagocytosis
