Final Exam Flashcards
what are the 4 characteristics of acquired immunity
- specificity
- diversity
- memory
- self/nonself recoginition
what are the 2 types of acquired immunity
- humoral immunity
2. cellular immunity
humoral immunity is caused by the action of __
antibodies
fights off foreign invaders
humoral immunity is mediated by __
b cells
cellular immunity is responsible for detecting __
self vs. non-self cell
cellular immunity is mediated by __
T cells
what is an antigen
it binds to antibody or t cell receptor to initiate acquired immune response
what are examples of lymphocytes
B and t cells
what is a hapten
it is a low MW substance that binds to a high MW substance to initiate an acquired immune response. but upon subsequent exposure, you don’t need the high MW substance
__ non specifically enhances immune response to antigens
adjuvant
for an antigen to be recognized by the immune system __
it has to be displayed with an MHC
what reduces the chance of an organ rejection
if the donor and host have similar MHC molecules
MHC class I deals with
recognizing altered-self cells
MHC class I are recognized by
T cytotoxic cells
__ cells are found on every cell
MHC class I cells
MHC class II are recognized by
T helper cells
MCH class II are only found on __
antigen presenting cells
how do MHC class II cells work
antigen will bind to MHC class II cells presented on the foreign cell surface
how does acquired immunity achieve its high specificity
by the formation of antibodies and t cell receptors
how are b and t cells different
b cells don’t require antigen presentation by MHC cells in order to be activated
__ stimulate B cells to allow them to proliferate to form
T helper cells stimulate B cell proliferation
memory B cells and plasma cells (effector cells)
what do memory b cells and effector cells do
memory b cells –> express membrane bound antibodies
effector cells–> produce soluble antibodies
describe the structure of antibodies
made of 2 heavy chains and 2 light chains
how can antibodies aid in the removal of pathogens
- agglutination - clump the particles together
- precipitation - complex of antibody and antigen become so large its no longer soluble
- neutralization - antibodies cover the active sites of foreign substance
- lysis - antibodies directly lyse the organism
T cells require __ to become activated
antigen presentation via a MHC complex
T helper cells recognize __
antigens presented on MHC class II molecules
in AIDS, __ are destroyed
t helper cells
what do T helper cells do
- stimulate b cell growth (humoral side)
- simulate Tc cells
- stimulate macrophages
- stimulate other Th cells
Tc cells interact with __
antigens presented on MHC Class I molecules
how are Tc cells activated
by T helper cells
what do cytotoxic T lymphocytes do
they secrete perforins which lyse cells (acts like MAC)
what is Type I hypersensitivity
it is IgE mediated
IgE binds to receptors on mast cells, resulting in sensitization of these cells
requires a second exposure
Type II hypersensitivity
antibodies destroy cells that present a foreign antigen (blood transfusions)
Type III hypersensitivity
auto immune disorder
Type IV hypersensitivity
T cell mediated
doesn’t involve antibodies
ex. poison ivy
after you cut yourself, the body does __ to prevent bleeding out
- constrict blood vessels
- form platelet plug
- blood coagulates
what are platelets
non nucleated fragments of megakaryocytes
platelets cannot __ because they are non nucleated
cannot proliferate
platelets secrete __
factors stored in granules once activated
what are the functions of platelets
- become platelet plugs
2. provide catalytic environment for the blood coagulation cascade
describe platelet activation
they become activated by exposure to ECM or soluble factors
change shape when activated and spread out to form platelet plug and provide catalytic environment
describe the steps of platelet plug formation
- platelets will adhere to the ECM
- They secrete factors for further platelet plug formation
- factors activate and attract more platelets which form an aggregate
- platelets express GPIIb/IIIa receptors for fibrinogen (fibrinogen allows platelets to stick together )
- platelets exhibit pro-coagulatory activity to further stabilize the plug
how can you determine if platelet activation had occurred
- look at how adhered the platelets are
2. look at how spread out they are
what are the parts of the coagulation cascade
intrinsic and extrinsic and common pathway
how does the intrinsic pathway start
trauma to blood vessels
requires exposed ECM (which is negatively charged)
describe the intrinsic pathway of the coagulation cascade
- factor 12 adsorbs to negatively charged surface and becomes activated
- factor 12a converts pre kallikrein to kallekrein and converts factor 11 to 11a
- kallikrein cleaves HMWK to form bradykinin
- ** bradykinin is an inflammatory mediator
- kallenkrien and factor 11a are bound to HMWK, which has high affinity for hydrophobic biomaterials (coagulation cascade will occur on hydrophobic biomaterials)
describe the extrinsic pathway of the coagulation cascade
- initiated by the release of tissue factor
- **tissue factor is released form macrophages or endothelial cells
- tissue factor complexes with factor 7 to anchor to the surface between membrane
which clotting pathway occurs first
extrinsic (occurs in about 15 seconds)
describe the common pathway of the coagulation cascade
- platelets secrete and have receptors for factor 5
- factor 5 will bind to factor 10a on the platelet surface
- factor 10a will cleave prothrombin into thormbin
- thrombin will cleave fibronigen to fibrin
- ** fibrin binds with fibrinopeptide A and B which are chemotactic for neutorphils
- thrombin also activates factor 13a
- factor 13a crosslink fibrin which will help stabilize the platelet plug
what are the ways to limit clot formation
- physiologic factors - high blood flow will prevent factors from being near each other
- heparin/antithormbin3 comples will bind to thrombins catalytic site and prevent the coagulation cascade
- thrombomodulin - bind to thrombin and prevent it from interacting with the rest of the cascade
- fibrinolysis - during clot formation, plasminogen gets trapped in the clot. TPA activates the plasminogen into plasmin which cleaves the fibrin fibers
what about the endothelium make it anti-coagulant
- heparan sulfate make the endothelium very smooth which prevents adsorption
- thrombomodulin is found on the surface
- they secrete TPA to dissolve clots
what about endothelium makes it pro-coagulant
- secretes cofactors in the extrinsic pathway
2. endothelium lining is disrupted, thus exposing the ECM which will start the intrinsic pathway
__ is the movement of a part of a clot into general circulation
embolization
problems with in vitro hemocompatability assays
- need to use anti-coagulants to preserve blood outside of the body
- must use pumps to circulate the blood
- need contorl surface (usually glass)
problems with in vivo hemocompatability assays
- animals have different blood composition than humans
2. difficult to control blood flow near implant
advantages of ex vivo hemocompatabiliy assays
- blood flow near implant can be controlled
- don’t need anticoagulants
- implants can remain in place for months
