Cells And Immune System - Topic 2 Flashcards
(20 cards)
What is phagocytosis?
A phagocyte (e.g. a macrophage) is a type of white blood cell that carries out phagocytosis (engulfment of pathogen).
1. A phagocyte recognises the foreign antigens (as it’s an abnormal protein) on a pathogen.
2. The cytoplasm of the phagocyte moves round the pathogen, engulfing it.
3. The pathogen is now contained in a phagocytic vacuole (a bubble) in the cytoplasm of the phagocyte.
4. A lysosome (an organelle that contains enzymes called lysozymes) fuses with the phagocytic vacuole. The lysozymes break down the pathogen.
5. The phagocyte then presents the pathogens antigens - it sticks the antigens on its surface membrane to activate other immune system cells.
How do phagocytes activate T-cells?
A T-cell (also called a T-lymphocyte) is another type of white blood cell. It has receptor proteins on its surface that bind to complementary antigens presented to it by phagocytes. This activates the T-cells. Different types of T-cells respond in different ways. For example helper T-cells release chemical signals that activate and stimulate more phagocytes and cytotoxic T-cells which kill abnormal and foreign cells. Helper T-cells also activate B-cells, which secrete antibodies.
How do T-cells activate B-cells?
B-cells (also called B-lymphocytes) are also a type of white blood cell. They’re covered with antibodies proteins that bind antigens to form an antigen-antibody complex. Each B-cell has a different shaped antibody on its membrane, so different ones bind to different shaped antigens.
1. When the antibody on the surface of a B-cell meets a complementary shaped antigen, it binds to it.
2. This, together with substances released from helper T-cells, activates the B-cell. This process is called clonal selection.
3. The activated B-cell divides into plasma cells.
How do plasma cells make more antibodies to specific antigens?
Plasma cells are identical to the B-cell (they’re clones). They secrete loads of antibodies specific to the antigens. These are called monoclonal antibodies. They bind to the antigens on yeast surface of the pathogen to form lots of antigen-antibody complexes.
An antibody has two binding sites, so can bind to two pathogen at the same time. This means that pathogen become clumped together - this is called agglutination. Phagocytes bind to the antibodies and phagocytose many pathogens at once. This process leads to the destruction of pathogens carrying this antigen in the body.
What are antibodies?
Antibodies are proteins - they’re made up of chains of amino acids. The specificity of an antibody depends on the variable regions, which form the antigen binding sites. Each antibody has a variable region with a unique tertiary structure (due to different amino acids sequences) that’s complementary to one specific antigen. All antibodies have the same constant region.
What are the two immune responses?
1) Cellular - The T-cells and other immune system cells that they interact with, e.g. phagocytes form the cellular response.
2) Humoral - B-cells, clonal selection and the production of monoclonal antibodies form humoral response.
How can the immune response memorise the antigens?
The primary immune response:
1. When an antigen enters the body for the first time it activates the immune system. This is called the primary response.
2. The primary response is slow because there aren’t many B-cells that can make the antibody needed to bind to it.
3. Eventually the body will produce enough of the right antibody to overcome the infection. Meanwhile the infected person will show symptoms of the disease.
4. After being exposed to an antigen, both T-cells and B-cells produce memory cells. These memory cells remain in the body for a long time. Memory T-cells remember the specific antigens and will recognise it a second time round. Memory B-cells record the specific antibodies needed to bind the antigen.
5. The person is now immune - their immune system has the ability to respond quickly to a second infection.
The secondary immune response:
1. If the same pathogen enters the body again the immune system will produce a quicker, stronger immune response - the secondary response.
2. Clonal selection happens faster. Memory B-cells are activated and divide into plasma cells that produce the right antibody to the antigen. Memory T-cells are activated and divide into the correct type of T-cells to kill the cell carrying the antigen.
3. The secondary response often gets rid of the pathogens before you begin to show any symptoms (you are immune to the pathogens).
How do vaccines protect individuals and the population against disease?
- While your B-cells are busy dividing to build up their number to deal with a pathogen (i.e. the primary response), you suffer from the disease. Vaccinations can help avoid this.
- Vaccines often contain antigens that cause your body to produce memory cells against a particular pathogen, without the pathogen causing disease. This means you can become immune without getting any symptoms.
- Vaccines can protect individuals that have them and because they reduce the occurrence of the disease, those not vaccinated are also less likely to catch the disease (because there are fewer people to catch it from). This is called herd immunity.
- Antigens in vaccines may be free or attached to a dead or attenuated (weakened) pathogens.
- Vaccines may be injected or taken orally. This disadvantages of taking a vaccine orally are that it could be broken down by enzymes in the gut or the molecules of the vaccine may be too large to be absorbed into the blood.
- Sometimes booster vaccines are given later on (e.g. after several years) to make sure that memory cells are produced.
How do antigenic variations help some pathogens evade the immune system?
- Antigens on the surface of pathogens activate the primary response.
- When you’re infected a second time with the same pathogen (which has the same antigens on its surface) they activate the secondary response and you don’t get ill.
- However, some sneaky pathogens can change their surface antigens. This antigen variability is called antigenic variation. (Different antigens are formed due to changes in the genes of a pathogen).
- This means that when you’re infected for a second time, the memory cells produced from the first infection will not recognise the different antigens. So the immune system has to start from scratch and carry out a primary response against these new antigens.
- The primary response takes time to get rid of the infection, which is why you get ill again.
- Antigenic variation also make it difficult to develop vaccines against some pathogens for the same reason. Examples of pathogens that show antigenic variation include HIV and influenza virus:
- The influenza vaccine changes every year. That’s because the antigens on the surface of the influenza virus change regularly, forming new strains virus.
- Memory cells produced from vaccinations with one strain of the flu will not recognise other strains with different antigens. The strains are immunologically distinct.
- Every year there are different strains of the influenza virus circulating in the population, so a different vaccines has to be made.
- New vaccines are developed and one is chosen every year that is the most effective against the recently circulating influenza viruses.
- Governments and health authorities then implement a programme of vaccination using the most suitable vaccine.
What is active and passive immunity?
- Active immunity = This is a type of immunity you get when your immune system makes its own antibodies after being stimulated by an antigen. There are two different types of active immunity:
1. Natural - this is when you become immune after catching a disease.
2. Artificial - this is when you become immune after you’ve been given a vaccination containing a harmless dose of antigens. - Passive immunity = This is the type of immunity you get from being given antibodies made by a different organism - your immune system doesn’t produce any antibodies of its own. Again, there are two types:
1. Natural - this is when a baby becomes immune due to the antibodies it receives from its mother, through the placenta and in breast milk.
2. Artificial - this is when you become immune after being injected with antibodies from someone else. E.g. if you contract tetanus you can be injected with antibodies against the tetanus toxin, collected from blood donation.
What are the difference between active immunity and passive immunity?
Active immunity:
- Requires exposure to antigen
- It takes a while for protection to develop
- Memory cells are produced
- Protection is long-term because the antibody is produced (after activation of memory cells) in response to complementary antigen being present in the body.
Passive immunity:
- Doesn’t require exposure to antigen
- Protection is immediate
- Memory cells aren’t produced
- Protection is short-term because the antibodies given are broken down.
What are monoclonal antibodies?
- Monoclonal antibodies are antibodies produced from a single group of genetically identical B-cells (plasma cells). This means that they’re all identical in structure.
- Antibodies are very specific because their binding sites have a unique tertiary structure that only one particular antigen will fit into (one with a complementary shape).
- You can make monoclonal antibodies that bind to anything you want e.g. a cell antigen or other substance, and they will only bind to (target) this molecule.
Example cancer cells:
1) Different cells in the body have different surface antigens.
2) Cancer cells have antigens called tumour markers that are not found on normal body cells.
3) Monoclonal antibodies can be made that will bind to the tumour markers.
4) You can also attach anti-cancer drugs to the antibodies.
5) When the antibodies come into contact with the cancer cells they will bind to the tumour marker.
6) This means the drug will only accumulate in the body where there are cancer cells.
7) So, the side effects of an antibody-based drug are lower than other drugs because they accumulate near specific cells.
Example pregnancy cells:
1) The application area contains antibodies for hCG bound to a coloured bead (blue).
2) When urine is applied to the application area any hCG will bind to the antibody on the beads, forming an antigen-antibody complex.
3) The urine moves up the stick to the test strip, carrying any beads with it.
4) The test strip contains antibodies to hCG that are stuck in place (immobilised).
5) If there is hCG present the test strip turns blue because the immobilised antibody binds to any hCG - concentrating the hCG-antibody complex with the blue beads attached. If no hCG is present, the beads will pass through the test area without binding to anything, and so it won’t go blue.
What is an ELISA test?
- The enzyme-linked immunosorbent assay (ELISA) allows you to see if a patient has any antibodies to a certain antigen or any antigen to a certain antibody.
- It can be used to test for pathogenic infections, for allergies (e.g. to nuts or lactose) and for just about anything you can make an antibody for.
- In an ELISA test, an antibody is used which has an enzyme attached to it. This enzyme can react with a substrate to produce a coloured product. This causes the solution in the reaction vessels to change colour.
- If there’s a colour change, it demonstrates that the antigen or antibody of interest in present in the sample being tested (e.g. blood plasma). In some types of ELISA, the quantity of this antigen/antibody can be worked out from the intensity of the colour change.
- There are several different types of ELISA. Direct ELISA uses a single antibody that is complementary to the antigen you’re testing for. Indirect ELISA is different because it uses two different antibodies.
Example HIV:
1) HIV antigen is bound to the bottom of a well in a well plate (a plastic tray with loads of little circular pits in it).
2) A sample of patients blood plasma,which might contain several different antibodies, is added to the well. If there are any HIV-specific antibodies (i.e antibodies against HIV) these will bind to the HIV antigens stuck to the bottom of the well. This well is then washed out to remove any unbound antibodies.
3) A secondary antibody, that has a specific enzyme attached to it, is added to the well. This secondary antibody can bind to the HIV -specific antibody (which is also called the primary antibody). The well is washed out again to remove any unbound secondary antibody. If there’s no primary antibody in the sample, all of the secondary antibody will be washed away.
4) A solution is added to the well. This solution contains a substrate, which is able to react with the enzyme attached to the secondary antibody and produce a coloured product. If the solution changes colour, it indicates that the patient has HIV-specific antibodies in their blood and is infected with HIV.
What are the ethical issues of vaccines and antibodies?
1) All vaccines are tested on animals before being tested on humans - some people disagree with animals testing. Also, animal based substances may be used to produce a vaccine, which some people disagree with.
2) Testing vaccines on humans can be tricky, especially, e.g. volunteers may put themselves at unnecessary risk of contracting the disease because they think they’re fully protected (e.g. they might have unprotected sex because they had a new HIV vaccine and think they’re protected - and the vaccine may not work).
3) Some people don’t want to take the vaccine due to the side effects, but they are still protected because of herd immunity - other people think this is unfair.
4) If there was an epidemic of a new disease (e.g. a new influenza virus) there would be a rush a receive a vaccine and difficult decisions would have to be made about who would be the first to receive it.
Ethical issues surrounding monoclonal antibody therapy often involves animal rights issues. Animals are used to produce the cells from which the monoclonal antibodies are produced. Some people disagree with the use of animals in this way.
What is HIV and how does it cause AIDS?
- HIV (human immunodeficiency) is a virus that affects the immune system. It eventually leads to acquired immune deficiency syndrome.
- AIDS is a condition where the immune system deteriorates and eventually fails. This makes someone with AIDS more vulnerable to other infections, like pneumonia.
- HIV infects (and eventually kills) helper T-cells, which act as the host cells for the virus. Remember helper T-cells send chemical signals that activate phagocytes, cytotoxic T-cells and B-cells so they’re hugely important cells in the immune response. Without enough helper T-cells, the immune system is unable to mount an effective response to infections because other immune systems cell don’t behave how they should.
- People infected with HIV develop AIDS when the helper T-cells numbers in their body reach a critically low level.
What is the structure of HIV like?
- A core that contains the genetic material (RNA) and some proteins (including the enzymes reverse transcription, which is needed for virus replication).
- An outer coating of protein called a capsid.
- An extra outer layer called an envelope. This is made of membrane stolen from the cell membrane of a previous host cell.
- Sticking out from the envelope are loads of copies of an attachment protein that help HIV attach to the host helper T-cell.
How does HIV replicate inside a host helper T-cell?
HIV (and all other viruses) can only reproduce inside the cells of the organism it has infected. HIV replicates inside the helper T-cells of the host. It doesn’t have the equipment (such as enzymes and ribosomes) to replicate on its own, so it uses those of the host cell.
1) The attachment protein attaches to a receptor molecule on the cell membrane of the host helper T-cell.
2) The capsid is released into the cell, where it uncoats and releases the genetic material (RNA) into the cells cytoplasm.
3) Inside the cell, reverse transcriptase is use to make a complementary strand of DNA from the viral RNA template.
4) From this, double-stranded DNA is made and inserted into the human DNA.
5) Host cell enzymes are used to make viral proteins from the viral DNA found within the human DNA.
6) The viral proteins are assembled into new viruses, which bud from the cell and go on to infect other cells.
How are AIDS susceptible to a range of illnesses?
People with HIV are classed as having AIDS when symptoms of their failing immune system start to appear or their helper T-cell count drop below a certain level. People with AIDS generally develop diseases that wouldn’t cause serious problems in people with a healthy immune system. The length of time between infection with HIV and the development of AIDS varies between individuals but without treatment it’s usually around 10 years.
1. The initial symptoms of AIDS include minor infections of mucous membranes (e.g. the inside of the nose, ears and genitals), and recurring respiratory infections.
2. As AIDS progresses the number of immune system cells decreases further. Patients become susceptible to more serious infections including chronic diarrhoea, severe bacterial infections and tuberculosis.
3. During the late stages of AIDS patients have a very low number of immune system cells and can develop a range of serious infections such as toxoplasmosis of the brain (a parasite infection) and candidates of the respiratory system (fungal infections). It’s these serious infections that kill AIDS patients, not HIV itself.
Why do antibiotics not work against viruses?
- Antibiotics kill bacteria by interfering with their metabolic reactions. They target the bacterial enzymes and ribosomes used in these reactions.
- Bacterial enzymes and ribosomes are different from human enzymes and ribosomes. Antibiotics are designed to only target the bacterial ones so they don’t damage human cells.
- Viruses don’t have their own enzymes and ribosomes - they use the ones in the host cells. So because human viruses are human enzymes and ribosomes to replicate, antibiotics can’t inhibit them because they don’t target human processes.
- Most antiviral drugs are designed to target the few virus-specific enzymes (enzymes that only the virus uses) that exist. For example, HIV uses reverse transcriptase to replicate. Human cells don’t use this enzyme so drugs can be designed to inhibit it without affecting the histamine cell. These drugs are called reverse-transcription inhibitors.
What is the best way to not spread HIV?
The best way to control HIV infection in a population is by reducing, it spreads. HIV can be spread via unprotected sexual intercourse, through infected bodily fluids (e.g. like blood from sharing contaminated needles) and from a HIV-positive mother to her foetus. Not all babies from HIV-positive mothers are born infected with HIV and taking antiviral drugs during pregnancy can reduce the chance of the baby being HIV-positive.
