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describe phagocytic cells (which immunity, how they affect microbes, and ways of killing)
these are second line innate immunity cells that kill microbes through lysosomes. the two ways of killing are when phagosomes go inside a lysosome and get killed. the other way is respiratory burst.
what make up phagocytic cells according to her slides?
macrophages, neutrophils, and dendritic cells
how do phagocytic cells know where to go? what do they need to do in order to eat?
they follow chemical trails through chemotaxis and opsonin’s tell them where to adhere to in order to begin “eating”
describe the phagosome + lysosome method (start with what is a phagosome)
a phagosome is anything that gets taken up in the lysosome. these lysosomes have hydrolytic enzymes inside that destroy microbes inside them. the membranes they’re made up by allow them to fuse with other lysosomes and safely transfer its contents. after digesting the contents, they will eliminate the waste out of the cell
describe respiratory burst
some pathogens can survive inside macrophages meaning there must be another way of killing them. respiratory burst kills them by creating Reactive oxygen species (ROS) likes superoxide, peroxide, and bleach to oxidize microbes and kill them.
what is a bacteria that needs to be killed through respiratory burst?
mycobacterium tuberculosis
what do natural killer cells have on them? (ligands)
activating and inhibitory ligands that determine whether a cell gets killed
what do normal cells have to let NKs know not to kill them?
they have reciprocating activating and inhibitory ligands
why do the normal cells not die if the activating ligand is also being bound together?
the inhibitory ligand most likely has a stronger response which tells the NK to not kill it
which ligand does a target cell not have to tell NKs to kill it and how does the NK kill it
they don’t have inhibitory ligands so the NKs tell them to kill themselves through apoptosisw
what are the two ways NKs kill target cells?
perforin and granzyme B
how does perforin work? granzyme b?
perforin is a glycoprotein that punctures holes into the membrane of the target cell. granzyme b is an enzyme that tells the target cell to kill itself through apoptosis
what were Natural Killer cells discovered for?
their ability to kill tumor cellswh
at is inflammation mediated by?
mast cells and basophils
what are the main symptoms of inflammation? (say why for each)
redness (presence of oxygenated blood)
heat (RBC movement)
swelling (liquid oozing out of relaxed blood cells)
pain (most likely pain of interstitial fluid pressing on nociceptors)
what are 4 steps of an inflammatory response? (thorn puncture)
Trauma/infection
the thorn enters the skin and presents microbes inside
then mast cells and phagocytes rush this area to eliminate foreign microbes
histamines are released from granulocytes
vasodilation
the histamine released causes the blood vessels to widen
this allows more antibodies and components to enter the tissue
phagocyte attraction
more phagocytes are recruited and go to the tissue and envelope microbes mainly targeted by opsonin’s
tissue repair
growth factors released by mast cells and macrophages promote healing of the tissue
what substance causes fevers?
pyrogens
what does fever do?
stimulates tissue repair (from needing to rest when sick)
inactivates toxins
inhibits microbial growth
increase phagocytosis
what are exogenous pyrogens
these are pieces of a microbe that causes a fever or LPS
what are endogenous pyrogens
pyrogens we make ourselves to cause fever
can fevers inactive exotoxins, endotoxins, or neither? why?
fevers can inactivate exotoxins because exotoxins are proteins but endotoxins are LPS
why does fever increase phagocytosis?
macrophages tend to work better at slightly higher temperatures
what are interferons?
these are communication systems that warns other noninfected cells that a cell is infected
steps of an interferon response for dsRNA
viral entry into a cell stimulates it to create interferons and release them from the cell to other cells. the viruses replicated from the infected cell go to the new cell but that cell has turned on genes to create antiviral proteins. these proteins then block viral synthesis of the virus
what IFNs are type 1
IFN alpha and beta
what IFNs are type 2
IFN gamma
what is the difference between IFN type 1 and 2
IFN type 1 warns against viruses and type 2 is produced by T lymphocytes and NK cells
what is the complement system?
these are proteins that work together to activate inflammation, activate chemoattractant (bring things in like immune cells), and kill certain microbes
what is the term for serum proteins activation?
a cascade
what are the three methods of activation
alternative - microbe directly
classical - antibody bound to microbe
lectin - lectin protein binding microbial carbohydrates
what do each of these methods all lead to?
c3 protein
what are c3 and c5a responsible for and what are they classified as?
they are responsible for inflammation and act as chemoattractants
what is c3b?
it is an opsonin
how does c5b, C6, 7, 8, and 9 all kill the cell? (what do they use)
they all use the membrane attack complex, or MAC
what are examples of lactoferrin?
milk
tears
sweat
blood
what are examples of transferrin
blood plasma and extracellualr fluids
what are the four ways iron-binding proteins are involved with pathogens?
pathogens uptake iron-binding proteins and destroy the protein to get the iron in order to grow
pathogens make siderophores to steal iron from the protein
some pathogens have hemolytic bacteria that collect hemoglobin from red blood cells through hemolysis
a small number of pathogens can trade the need for iron with Mg
how does the immune system know theres an infection?
microbes have pathogen associated molecular patterns which trigger the immune system.
what are the limits of PAMPs?
PAMPs can detect the type of infecting microbe
the body has microbes with PAMPs, why doesnt the body attack those ones?
for the immune system to react it has to be immune system + damage
toll-like receptors are a family of what?
PRRs
do all cells of the body have PRRs for viruses?
yes