immunity (quiz 9) Flashcards
1st step of immune response
neutrophils and macrophages recognize PAMPs on foreign bodies via PRR
invaders are destroyed by phagocytosis or inflammation
upon failure, adaptive immune system is “recruited”
2nd step of immune response
DCs take up antigen and bring to lymph nodes for presentation to adaptive immune system
3rd step of immune response
DCs present antigen to T-cells
4th step of immune response
T/B-cells leave lymph nodes and travel to infection sites
CD8 T-cells go kill
CD4 T-cells prime more T/B-cells for immune response
PAMP
PRR
DC
MHC Class 1
CD8; cytotoxic T-cells
MHC Class II
CD4; helper T-cells
Post-infection
Regulatory T-cells and suppressive cytokines stop inflammation and immune response
Memory T/B-cells are created (adaptive immunity)
“hot” tumor
immune cells recognize tumor as enemy; eliminates
“cold” tumor
immune cells do not recognize tumor; allows for tumor growth
cold immunotherapy
adoptive t-cell transfer, boosting immune response, vaccines
step 1 of immunoediting
tumor becomes invisible;
MHC class I goes down,
co stimulatory molecules decrease
step 2 of immunoediting
cancer cells resist apoptosis;
anti-apoptotic proteins (Bcl-2) raise
P53 lowers
Fas lowers
step 3 of immunoediting
begin to kill immune cells;
fasL goes up
TRAIL goes up
step 4 of immunoediting
suppresses immune sys;
secretes variety of different factors
exploits immune checkpoints
step 5 of immunoediting
sabotages immune cells to work for the tumor;
secretes regulatory T-cells
MDSC
M2/N2
IDO
Possible mechanisms to cure cancer
Vaccines
Adoptive t-cell transfer
Blocking immuno suppression
(VAB)
blocking immunosuppression
anti-CTLA-4
anti-PD-1
function of CTLA-4
allows t-cell binding to dendritic/B-cells
function of PD-1
allows tumor to bind with effector T-cells (CD8)
process of blocking immunosuppression
- APC containing TAA > lymph node
- T-cells are primed with TAA
- T-cells migrate to cancerous tissue, destroy it
*approved w melanoma
T-cell transfer (autologous)
- part of tumor is removed
- TIL are isolated and grown
- TILs are infused with IL-2
T-cell transfer (genetically engineered)
- lymphocytes in blood are isolated
- retrovirus inserts TCR gene
- cells are genetically engineered to grow a shit ton
- cells are infused w IL-2
infammasome
heating up cold tumors
platelet plug formation
caused by vasoconstriction and aggregation of platelets
platelet plug formation
platelets bind to collagen (vWF), change shape
hemostasis
stopping bleeding
how do platelets change surface area
binding with von Willebrand Factor (vWF)
Alpha granules
secrete growth factor
long-term wound healing
dense granules
release ADP n Make thromboxane (TXA2)
ADP
binds to P2y12, further activates platelets
TXA2
binds to TP, further activates platelets
fibrinogen (liver)
causes platelets to adhere to each other
proteins in platelets that make them contract
actin and myosin
generation of thromboxane
COX (cyclooxygenase)
thromboxane synthase
how long do platelets circulate?
7-10 days
what removes platelets from blood stream?
spleen
what produces platelets?
bone marrow
whats the first thing that happens when a platelet is activated?
becomes dendritic
what happens when a platelet becomes dendritic
releases cytokines, chemokines, and pro-coagulation factors
hemostasis steps
- severed vessel
- platelets agglutinate
- Fibrin appears
- fibrin clot forms
- clot retraction occurs
what cleaves fibrin into monomers
thrombin
what do fibrin chains do?
stabilizes platelet plug
fibrinolysis
plasma proteins get trapped in clot; prevents them from destroying it
what happens after the clot has stopped the bleeding
t-PA converts plasminogen to plasmin; removes unnecessary blood clot
allows for small vessels that were previously blocked to be reopened
thrombus
blood clot
thromboembolism
thrombus detatching from either the vessel or a biomaterial
biofouling
harm the patient or cause dysfunction of implanted device
types of biofouling
thrombosis
biofilm formation (extracellular polymer on material)
