immunity Flashcards
what is a lymphocyte
white blood cell involved in immune responses
what is self antigen
a molecule on the cell surface membrane of a body cell that does not usually trigger an immune response
what is immunity
the means by which the body protects itself from infection
what is a foreign antigen
a molecule on the cell surface membrane of a foreign cell that triggers an immune response
what is a pathogen
a disease causing microorganism
what is a non specific defence mechanism
give examples
response is immediate and the same for all pathogens
skin
phagocytosis
what is a specific defence mechanism
give examples
response is slower and specific
cell mediated response - t cells
humoral response - b cell
how is skin a non specific mechanism
has a flat outer layer of dead cells consisting of keratin protein which makes a tough barrier
keratin is a fibrous protein which has a;
repetitive primary structure sequence
errors have less impact on function
few tertiary bonds
how is cilia a non specific structure
they are in your nose and covered in mucus produced by goblet cells
cilia waft pathogens trapped in the mucus up the throat to be swallowed
how is stomach acid a non specific structure
kills pathogens by denaturing proteins in bacterial cell wall or outer layer of virus
how is lysosomes a non specific structure
in your tears
enzyme which digests the cell wall of bacteria
what is a phagocyte and what types can it be
phagocyte is a special type of leukocyte which can engulf pathogens
they travel via bloodstream but can migrate to other tissue
it can be a macrophages - patrols around the body and lasts a long time
or
neutrophil - lasts 7 days
what is histamine and what does it do
chemical which is released by damaged tissues (cuts)
this causes the blood vessel to dilate and helps to speed up arrival of phagocytes to the area
what is an antibody
protein synthesised by plasma cells with a specific tertiary structure that is complementary to an antigen so they can bind to form an antigen antibody complex
describe phagocytosis
1.cytokines produced by pathogen attract phagocyte towards pathogen
2.phagocytes attach themselves to the surface of the pathogen
3. phagocytes engulf the pathogen to form a vesicle called a phagosome
4.lysosomes containing hydrolytic enzymes fuse with phagosome
5.enzymes hydrolyses phagosome and digests it
6.soluble products from the hydrolysed pathogen are absorbed into the phagocyte
7. antigens are presented on the cell membrane
8. inflammation occurs because histamine in the area has puss made of dead and digested pathogens and phagocytes
where does a t lymphocyte mature
what does it do
thymus gland
it does cell mediated responses and does NOT secrete antibodies
where does a b lymphocyte mature
what does it do
bone marrow
humoral response does secrete antibodies
why does your body not fight its own cells
they have highly specific tertiary structure proteins which lymphocytes will recognise
what are the two types of leukocyte
phagocyte and lymphocyte
what are the two types of lymphocyte
T and B
what does a phagocyte do
phagocytosis
what does a B lymphocyte make
B memory cells and plasma cell
what does a B memory cell do
remember antigens for next time
what does a T memory cell do
remember antigens for next time
what do T lymphocytes make
T suppressor cells
T helper cells
T memory cells
T cytotoxic cells
what does a T suppressor cell do
stops an immune reaction
what does a T helper cell do
produces cytokynes to attract other cells and activate phagocytosis and activate clonal selection and expansion
what does a T cytotoxic cell do
kill infected host cells by perforating the membrane so osmosis can happen
what is clonal selection and expansion
selection - looking for the right cells complementary to antigen
expansion - relevant cells divide by mitosis
describe the steps of a humoral response
1.pathogens circulate the blood stream and phagocytosis occurs
2. pathogen antigens also circulate the blood stream
3. specific B lymphocytes engulf pathogenic antigens
4. foreign pathogen are displayed on surface of the B lymphocytes
5. activated T helper cells bind to presented foreign antigen
6. activated T helper cells activate one B lymphocyte to divide via mitosis
7.the clones differentiate to form plasma B cells and B memory cells
8. plasma cells produce antibodies
9. the antibodies bind with antigens on invading pathogens
10. memory B cells remain for next time
what is agglutination
binding antigens together so that phagocytosis can happen quicker ( so they can be engulfed easier)
what is opsonisation
antibodies binds to antigens and receptor on the surface of pathogen
describe the structure of an antigen
Y shaped protein secreted by plasma b cell
made of 4 polypeptide chains - 2 heavy , 2 light
variable region is specific to antibody
describe how a monoclonal antibody test works
antigen is attached to the well of a dish
sample of blood is added ( if antibodies are present they will bind )
wash out the well
add a second antibody and enzyme which binds to specific antibody
wash out well
add a solution which will make the enzyme a colour to show if antibodies are present
how can monoclonal antibodies be used for cancer treatment
bind to cancer and block chemical signals which stimulate uncontrollable growth
radioactive substances can be attached to antibodies and delivered to specific site
What diseases can monoclonal antibodies be used to diagnose
influenza
hepatitis
chlamydia
how can monoclonal antibodies be used for pregnancy tests
allows early detection at home
rely on placenta producing HCG which is detected in urine which moves along the stick until antigens catch on antibodies making a white line
how are monoclonal antibodies made
mouse if exposed to something causing antibodies to be made by the B cells
these are collected and mixed with a tumor cell to make them reproduce rapidly
detergent is added to break down cell surface membrane so they fuse together making hybridoma cell
the cells are then separated and any clone producing the antibody are made on a large scale
antibodies are then extracted
ethical issues with monoclonal antibodies
deliberately stimulating tumor cells in mice
how does the quantity and speed of antibody production change after 2 injections
primary response produces less antibodies at a slower rate because clonal selection and expansion is slower
secondary response is quicker and produces more antibodies because memory cells speed up clonal selection
what is a vaccine
injection of antigens or attenuated microorganisms that have been treated in some way to make them harmless
stimulates the formation of memory cells
how does a vaccine stimulate the formation of memory cells
macrophage engulf the pathogens and present it as an antigen presenting cell
then the cell goes through clonal selection where T helper cells release cytokines to attract complementary B cells
the correct B cells then go through clonal expansion via mitosis and then differentiate to produce memory cells
what is passive immunity
injection of antibodies
short lived
antibodies not replaced by the person’s immune system
what is active immunity
injection of antigens
produces antibodies actively
long lasting immunity
antibodies replaced by person’s immune system
what is herd immunity
when a sufficiently large proportion of the population has been vaccinated against a disease making it difficult for a pathogen to spread
5 reasons why vaccines rarely eliminate disease
people with defective immune systems fail to induce immunity
people can develop the disease immediately after the vaccine and infect people
pathogens mutate frequently
different varieties of disease
objections to individuals
ethics of injections
risk to the individual who is having the vaccine
should expensive vaccine programs be carried out if disease is almost eradicated
is it fair to test new vaccines with unknown health risks only in a country where the target disease is common
animals involvement in vaccine development
should they be compulsory
describe how HIV replicates
1.HIV is in the blood
2.attachment proteins bind to CD4 on T helper cell
3. capsid fuses with cell membrane RNA and reverse transcriptase enter
4. DNA made from RNA using reverse transcriptase
5. DNA moves into nucleus via pores
6. virus DNA transcribed to MRNA
7. MRNA diffuses out of the nucleus
8. protein synthesis occurs to make HIV proteins
9. HIV particles break off
exocytosis releases it into the blood
why are people with HIV at greater risk from infectious diseases
it damages their T helper cells which means the patient is unable to produce cytokines , activate phagocytosis and clonal selection/ expansion
explain why AIDS leads to death
patients are more at risk from other diseases especially influenza , cold and TB
they don’t have enough T helper cells so the pathogens damage the cells , tissues and organs and release toxins
how is HIV treated and controlled
no cure
meds can slow the spread around the body by stopping the pathogen replicating so quickly
how is HIV transmitted
unprotected sex
sharing needles between intravenous drug users
infected mothers across the placenta
blood transfusions
why are antibiotics ineffective against viruses
they inhibit enzymes making mirin in the cell walls - viruses don’t have cell walls
they inhibit DNA replication- viruses don’t have DNA
