Cell recognition and the immune system Flashcards
Pathogen
Infectious organisms which spread communicable diseases are known as pathogens
Pathogens include bacteria, viruses, fungi and protoctista: the type of pathogen determines how it spreads
Vector
A vector is something which carries a pathogen from one organism to another
Antigen
Antigens are molecules present on the surface of cells, which trigger an immune response
The effect of antigen variability on disease and disease prevention
Reduces the effectiveness of vaccines
Antigenic drift/Antigenic shift
Antibodies are no longer complementary to antigens/don’t bind
Phagocytosis
- Chemotaxis - phagocyte attracted to pathogen by chemical products (toxins) from the pathogen. Moves towards pathogen along concentration gradient
- Phagocyte has several receptors on cell surface membrane that attach to chemicals on the surface of the pathogen
- Lysosomes move towards the phagosome being formed (an engulfed pathogen forms a vesicle called a phagosome) as the phagocyte engulfs the pathogen
- Hydrolysis - the Lysosomes release lysozyme’s into the phagosome, where they hydrolyse the pathogen
- The Hydrolysis products are absorbed by phagocyte
Describe the response of T lymphocytes to a foreign antigen
1) Pathogens are taken in by phagocytes after invading body cells.
2) The phagocyte places antigens from the pathogen on its cell-surface membrane.
3) Receptors on the specific helper T cell fit exactly onto these antigens.
4) This attachment activates the T cell to divide rapidly by mitosis and form a clone of genetically identical cells.
The cloned T cells:
a) develop into memory cells that enable a rapid response to future infections by the same pathogen.
b) stimulate phagocytes to engulf pathogens by phagocytosis.
c) stimulate B cells to divide and secrete their antibody.
d) activate cytotoxic T cells.
The role of antigen-presenting cells in the cellular response
An APC presents antigens to helper T cells to activate the T cells during a cellular response
The role of helper T cells (TH cells) in stimulating cytotoxic T cells (TC cells), B cells and phagocytes
Helper T cells attach to phagocyte which activates it to clone by mitosis
The cloned T cells activate cytotoxic T cells, stimulate B cells to divide and secrete their antibody and stimulate phagocytes to engulf pathogens by phagocytosis
Antibody
Antibodies are proteins with specific binding sites synthesised by B cells
Antibody structure
Made up of 4 polypeptide chains
The chains of one pair are long and are called heavy chains, while the chains of the other pair are shorter and are light chains
Each antibody has a specific binding site that fits exactly onto a specific antigen to form an antigen-antibody complex
The binding site is different on different antibodies and is called the variable region - consists of a sequence of amino acids that forms a specific 3D shape that binds directly to a specific antigen
The rest of the antibody is the constant region which binds to receptors on B cells
The formation of an antigen-antibody complex, leading to the destruction of the antigen, limited to agglutination and phagocytosis of bacterial cells
Once made, antibodies function by:
Binding to antigen on pathogen and acting as a marker/opsonin, making the entire antibody pathogen complex more likely to be phagocytosis than the pathogen alone would be
Binding to antigen on multiple pathogens and clumping pathogens together (agglutination), again making pathogens easier to phagocytose
The roles of plasma cells and of memory cells in producing primary and secondary immune responses
When a person is initially exposed to an antigen, the immune response occurs to produce plasma cells (which produce antibodies) to destroy the antigen
This is called the primary response
The primary response generates memory cells, so that if the same antigen is encountered again, the memory cells will rapidly produce many antibodies to destroy the antigen
This is called the secondary response and:
1. Is faster -> antibodies more produced after a short period of time after infection
2. Leads to antibodies being produced more quickly after they start being produced
3. Leads to a greater total number of antibodies being produced
As such the pathogen is destroyed before symptoms develop
Memory cells can circulate in the blood stream for years of they provide long-term immunity from the original infection -> this is natural, active immunity
The use of vaccines to provide protection for individuals and populations against disease
If a person is artificially exposed to an antigen (in a vaccine) the immune response is simulated and thus the response of memory cells so then if the person is exposed to the antigen in future they will become immune to it
Artificial, active immunity
1. Vaccine contains antigens from pathogen
2. Macrophage carries out phagocytosis of antigen, then displays antigen on its surface, acting as an antigen presenting cell
3. Specific T helper cell with complementary receptor will bind to protein and stimulates specific B cell
4. B cell divides by mitosis then differentiates to form plasma cells and memory cells
5. Plasma cells produce and secrete antibodies with binding site complementary to antigen
Vaccination is particularly useful for highly pathogenic disease which may cause a lot of damage/death if contracted
Usually made of dead or attenuated pathogens or isolated antigen proteins from their surface
Herd immunity
A pathogen must be passed from host to host to survive in the population
If the majority of the population are immune to a pathogen, it cannot spread, meaning the whole population is protected, even including those who are not yet vaccinated
The proportion of the population who need to be vaccinated to achieve herd immunity varies from pathogen to pathogen (depending how quick it is to spread)
The differences between active and passive immunity
- Active involves memory cells, passive does not
- Active involves production of antibody by plasma cells/memory cells
- Passive involves antibody introduced into body from outside/named source
- Active long term, because antibody produced in response to antigen
- Passive short term, because antibody (given) is broken down
- Active (can) take time to develop/work, passive is fast acting
Structure of HIV and its replication in helper T cells
- RNA (as genetic material)
- Reverse transcriptase
- (Protein) capto eres/capsid
- (Phospho)lipid (viral) envelope OR envelope made of membrane
- Attachment proteins
Viruses cannot replicate themselves but enter a host cell and uses its organelles to replicate
HIV attached to a protein called CD4 on the surface of T-helper cells; the capsid fuses with the cell membrane and the RNA and enzymes enter the cell
Reverse transcriptase copies the RNA into DNA. DNA enters the nucleus (via the nuclear pore) and is inserted into the host DNA
The DNA may remain dormant in this state without replicating for many years
The person is HIV positive but has not yet developed AIDS
When the virus starts replicating the DNA is transcribed into mRNA, then the mRNA is translated by the ribosomes to assemble the viral proteins
These assemble into new HIV particles, which break out of the cell, taking a section of plasma membrane with them to form the lipid coat
Once the virus starts replicating it destroys the T-helper cells (or prevents their normal functions)
Without T-helper cells, B-cells are not stimulated to make antibodies and cytotoxic T cells are less effective at killing virus-infected cells
The immune response is drastically reduced, leaving the person less able to destroy other pathogens and therefore more susceptible to all infections
Therefore the individual may then develop many different infections which will eventually lead to death
AIDs is typically diagnosed by identifying AIDs-related symptoms and by analysing the number of T helper cells in an individuals bloods
AIDs cannot be detected by using an ELISA as there are no antigens to detect
HIV can only be detected in this manner
Why antibiotics are ineffective against viruses
Antibiotics work by disrupting the cellular processes of bacteria
HIV is a virus so uses the host cell to replicate and has no cellular processes of its own
When inside the T helper cell antibiotics cannot reach it
Antibiotics are ineffective against viruses
Drugs which are helpful against HIV are called antiretroviral drugs
which prevent the virus from replicating so the T helper cells are not destroyed
With effective ARVs a HIV positive person can now expect a normal life span
The use of monoclonal antibodies in:
- targeting medication to specific cell types by attaching a therapeutic drug to an antibody
- medical diagnosis
Details of the production of monoclonal antibodies is not required
Monoclonal antibodies -> antibodies with the same tertiary structure and therefore the same shape binding site, produced from identical B cells or plasma cells
Targeting medication to specific cell types:
Monoclonal antibodies with a binding site known to be complementary to antigen found on a specific cell type can have a therapeutic drug attached to them
The antibodies will bind to this type of cell, delivering the drug to this specific location
Medical diagnosis (e.g. pregnancy testing)
Placenta produces a hormone called hCG (human chorionic gonadotrophin) which is found in the mother’s urine
Pregnancy test strip contains monoclonal antibodies which bind to this hormone, each with a coloured particles attached
The antibody-hCG complexes move along the strip and bind to a second hCG antibody which is fixed in place so the coloured particles are concentrated in this area and appear as a line (usually blue) on the strip
Ethical issues associated with the use of vaccines and monoclonal antibodies
Vaccines save millions of lives
BUT
Production of vaccines often uses animals
Side effects must be balanced against benefits
The use of antibodies in the ELISA test
Specific e.g. of the use of monoclonal antibodies for medical diagnosis -> in this case monoclonal antibodies are used to identify the presence of a specific antibody in the blood
- The pathogen’s antigen is placed and bound in a well
- The patient’s antibodies from their blood is added to the well
Any antibodies which are complementary to the antigen will bind to the antigen - The well is washed to remove any unbound antibodies
(This makes sure that unbound antibodies aren’t left in the well which could cause a false positive) - Monoclonal antibodies with an enzyme attached to them are added
These monoclonal antibodies have a binding site complementary to the antibody which you are trying to detect
The monoclonal antibodies will bind to any of the first antibodies bound to the antigen - The well is washed again to remove any unbound monoclonal antibodies.
- A colourless substrate is added that the enzyme attached to the monoclonal antibodies will cause to react and produce a coloured product, leading to a colour change
If the test is negative there would be no colour change as there would be no specific antibodies for the secondary antibodies to bind to
Make sure to revise the different types of ELISA testing
e.g. direct, indirect and sandwich
Evaluate methodology, evidence and data relating to the use of vaccines and monoclonal antibodies
If evaluating use of vaccines, consider:
Sample size
How many people were involved?
Is it a small sample size?
Was there a mix of people of different ages and from different ethnic groups?
If not, are the results representative of the entire population?
Control variables.
Were the people in the trial the same age/health?
Could any other variable have affected the data?
Stats test.
Has one been carried out?
What does this mean?
(If appropriate) correlations.
Is it strong or weak?
(If appropriate) SD bars.
Are they big or small?
Do they overlap or not?
What does this mean?
Monoclonal antibodies -> need to carefully balance potential medical value against objections and risks to make informed decisions about the use of monoclonal antibodies
If considering a trial consider sample size, control variables, results or absence of stats tests as part of evaluation of data
