IHL I - Innate Immunity Flashcards
receptors for innate immunity
no recombination
innate immunity
has no memory!
nonclonal
identical receptor on all cells
neutrophils
primary responder
phagocytic
shortlived
granular
aka PMNs
component of PUS
whats in granules in neutrophils
lysozyme collagenase elastase defensin cathelicidins
Cā
complement abbreviation
receptors on neutrophils
IFN-gamma chemokines TLRs C' mannose scavenger FcR IgG
macrophage
mature in the tissues
2 types
resident
inflammatory
phagocytic
large, granular, amoeboid, long lived in tissues
activated macrophage?
phagocytosis opsonization ROS iNOS cytokines growth factors
resident macrophages
live in tissues permanently
surveillance of tissues
kupffer
liver macrophages
osteoclast
macrophage in bone
recruited macrophage types
**inflammatory
antigen non-specific
alternatively antigen
classically antigen activated - migrates to sites of inflammation**
microglia
macrophage in CNS
natural killer cells
lymphoid progenitor cells
recognized bad cells and kill them
secrete IFN-gamma - activate macrophages
activated by IL-12 (From macrophages)
inhibitory receptor class I MHC
IFN -gamma
activates macrophages
secreted by NK cells
granzymes and performins
released by NK cells that lead to apoptosis
main antiviral defense?
type 1 IFN and NK cells
cooperativity between NK cell and macrophage
IL-12 activates NK cells (from macrophage)
IFN-gamma activates macrophages ) from NK cells
receptors on NK cells
activating and inhibiting receptor
normal cells constitutively have activating ligand and inhibiting ligand
viruses downregulate the class I MHC negative (inhibiting ligand)
mast cells
granules of histamine
two types:
tissue
mucosal
resident in tissue
-disruption releases lots of stuff
eosinophils
differentiate in response to IL-5
combat multicellular parasites (not many in the US)
like mast cells
dendritic cells
APCs (antigen presenting cells)
at first phagocytose, then antigen presenting
two types:
- conventional - plasmacytoid
bridge between innate and adaptive immunity
epithelia
physical barrier stratified squamous with the tight junction
have flora that are actually defensive
intraepithelial lymphocytes
produce antibiotics - defensins
mucosal surfaces
rapid pH changes
mucus traps thing - cilia move it out
have normal flora
defensins
very small <100 AAs
positive charge
beta sheets - 6 disulphide bonds
antimicrobial activity of defensins
gram - and + bacteria
parasites
fungi
viruses
produced by neutrophils, lymphocytes, paneth cells, epithelial cells, keratinocytes
cathelicidins
similar to the defensins
PAMPs
structure shared by microbes
not present on self
things that the pathogen cannot mutate without killing themself
DAMPs
damage associated molecular patterns
released by stressed cells
TLRs
toll like receptors
signaling through NF-kB
upregulate: TNF, IL-1B, IL-6, IL-8, IL-12
NOD receptors
intracellular TLRs
involved in inflammasome
innate immune evasion
bacteria have found ways to evade our immune response
omphalitis
umbilical stump inflammation
rebuck skin window
scrape skin
put cover slip on
look for neutrophils and macrophages
leukocyte adhesion deficiency
negative rebuck skin test
three process of acute inflammatory response
vasodilation
increased vascular permeability
emigration of leukocyte from blood into damaged areas
edema
brings plasma proteins to the damaged area
clotting, fibrinolytic, Cā, kinins
LAD
leukocyte adhesion deficieny
autosomal recessive
