Immune System Flashcards
Antigen
A protein on the cell surface which recognises it as a non-self molecule which then causes an immune response
Pathogen
A micro organism that causes disease
Phagocytosis
Bacterium relases chemoattractants for the phagocyte to follow
Foreign antigens bind to the surface ignorer for the phagocyte to engulf the bacterium
Bacterium becomes a vesicle with a protective layer
Phagosome
Lysosomes fuse and inject into the phagosome
Phagolysosome
Lysosomes release digestive hydrolytic enzymes which break down and destroy the phagolysosome
Exocytosis
Immune Response
Pathogen Antigne Phagocyte Antigen Presenting Cell T-Lymphocytes B-Lymphocytes Memory B Cells Plasma Cells Antibodies
T-Lymphocytes
Divide by mitosis create clones memory T cells cytotoxic T cells B cells
B-Lymphocytes
Divide by mitosis
create clones
memory B cells
plasma cells
Plasma Calls
Create antibodies
Antibodies
proteins 4 polypeptide chains -2 long and heavy -2 short and light variable region is specific to an antigen
Antigen-Antibody Complex
Antigen-Antibody Complex
Do antibodies destroy pathogens?
Antibodies do not direvtly destroy pathogens they just prepare them for destruction
Agglutination
cause microbes to clump together
act as markers
Neutralisation
some pathogens produce toxin
antibodues nautralise these toxins
Viruses
proteins on their surface bind to receipts on the host cell
this is how they enter the cell
Antibodies stop viruses binding to host cells so they can not enter
Polyclonal Antibodies
when different types of antiobodies are produced by one pathogen
How to create Monoclonal Antibodies
Inject specific antigen into mouse
Stimulating the prodocudtion of plasma cells
Plasmas cells are removed and fused with cancerous myeloma cells
Hybridoma cells are formed which are immortal and divide infinetly
Producing a single type of antibody
Uses of Monoclonal Antibodies
Use in treatments of cancer
Medical diagnosis
Pregnancy testing
Problems with Monclonal Antibodies
As we use mice their antibodies might be too different and recognised as foreign in our own body which will trigger and immune response
quickly inactivating the mAbs
How to minimise mAbs risk
geneticaly engineering the mAbs inorder to humanise them
Ethics of mAbs
Involes using mice or rabbits which deliberatly induces cancer in them
leads to suffering and death
Safety of mAbs
there have been associated deaths
not all good ecperineces in testing
can cause long term health problems
Direct Cancer Treatment
mAbs specific to the antigens on cancer cells are produced
Antibody binds to cancer call and blocks chemical signals
that stimulate growth
Indirect Cancer Treatment
radioactive/cytotoxic drugs are attached to the antibody
antibody binds to the recpetor on the cancer cell
call is killed
ADEPT
Antibody Dependent Enzyme Prodrug Therapy
using antibodies complemetary to specific pathogens in the blood to detect their presence
Pregnancy testing
mAbs antibody complementary to HCG (only detected during pregnancy)
mAbs attaches to HCG and pulls it down
B and T Lymphocytes Activation
B cell triggered when it encounters matching antigen
B cell engulfs the antigen and displays fragments of its MHC molecule
Antigen and MHC combination attracts mature matching T call
T cells secrete cytokinesis which actiavtes B cells to multiply and mature
Plasma cells
Released into the blood
Antigen-Antibody complexes cleared by the complement cascade.
Vaccine
preperation of antigen
injected or given by mouth
antigen from vaccine enters body
stimulates primary immune response
Clonal Selection
Antigens bind to complemetary glycoprotein on B and T lymphocytes
Stimulates immune response
Clonal Expansion
B and T lymphocytes dic=vide by mitosis
Primary Immune Response
B lymphocytes activate plasma cell production
Antibodies produced to neutralise or agglutinate pathogens
Takes a few days for antibody numbers to rise in blood
Same process occurs whether it is naturally or a vaccine
Secondary Immune Response
B memory cells circulate in the blood
Upon antigen binding they rapidly divide by mitosis to give plasma cells
Antibodies are produced faster than in the primary and there is no need for T cell actiavtion
Rapid response to the antigen
Vaccination
Antigen stimualte primary response Specific B cells bind to antigens Actiavtes by T helper cells B cells divide by mitosis to produce plasma cells and memory cells Plasmas cells produce antibodies Neutalise infection Memory cells encounter antigen Stimulates secondary rsponse Much faster
more vaccines boost levels of memory cells
Natural Immunity
Biological process
Artificial Immunity
scientific/medical process
Active Immunity
Lymphocyte receptors actiavted by antigens
Passive Immunity
no lymphocytes are activated
Natural Active
long term
infected by disease causing an immune response
takes time
Natural Passive
Immediate protection
antibodies from mother (across placenta) or (breast milk)
short term immunity
Artifical Active
long term immunity
immunisation or vaccination
takes time
Artifical Passive
immediate protection
injected with antibodies (tetanus injections)
short term immunity
Immunodeficinecy
They dont have an immune system so giving them a vaccine could kill them.
They can’t fight off the infection.
Herd Immunity
if almost eveyone in the population is vaccinated
it is unlikely the small amount of people who arent will become infected
There is no one to pass on the infection and nowhere for it to live
Antigenic Variation
Pathogens can slightly change their surface antigens
Upon secondary infection memory cells do not recognise the antigens
Vaccine development beomes difficult
