Immunity Flashcards
(65 cards)
1
Q
What is a pathogen?
A
A microorganism that causes disease.
2
Q
DEFENCE MECHANISMS - non-specific
A
- response is immediate and the same for all pathogens
- Physical barrier - e.g. skin and mucus. Prevents pathogens from entering the body.
- Phagocytosis - phagocytes engulf and destroy pathogens
3
Q
DEFENCE MECHANISMS - specific
A
- response is slower and specific for each pathogen
- Cell-mediated response - T lymphocytes - can hunt down and destroy infected/mutated cells.
- Humoral response - B lymphocytes - secrete antibodies
4
Q
Explain cell-surface antigens
A
- cell-surface membranes contain protein molecules and glycoproteins
- these vary between organisms and the different types of cell in an organism.
- they are known as cell-surface antigens
- your own cell-surface antigens identity your cells as ‘self’
- foreign material has antigens that are different, so they are ‘non-self’
5
Q
What is an antigen?
A
A foreign protein on the surface of something (e.g. a cell) that stimulates an immune response.
6
Q
Where are antigens found?
A
- pathogens
- abnormal body cells (e.g. cancer cells)
- toxins
- cells from other individuals of the same species (e.g. transplants)
7
Q
Explain the process of phagocytosis
A
- Phagocyte recognises the foreign antigen on a pathogen (because it is attracted to the chemicals produced and they move up the the chemical gradient).
- The cytoplasm of the phagocyte moves around the pathogen, engulfing it, as the phagocyte has receptors on its cell surface membrane which attach to the chemicals on the surface of the pathogen. This forms a phagosome.
- A lysosome (containing enzymes called lysozymes) fuses with the phagosome, and releases their lysozymes into the phagosome, which hydrolyse the pathogen.
- The soluble products from the breakdown of the pathogen are absorbed into the cytoplasm of the phagocyte.
- Anything that is not soluble or cannot be used by the cell is released by exocytosis.
8
Q
LYMPHOCYTES - B lymphocytes
A
- mature in the bone marrow
- lead to the production of antibodies
9
Q
LYMPHOCYTES - T lymphocytes
A
- mature in the thymus glad and are involved in cell-mediated immunity
- destroy infected cells and activate other cells
10
Q
How do we get antigen-presenting cells?
A
When a phagocyte destroys a pathogen, it presents and exposes the antigens on their cell-surface membrane.
Infected cells (e.g. by a virus) could also present antigens.
11
Q
What antigens do T lymphocytes respond to?
A
Only to antigens that are presented on a body cell (as opposed to antigens within body fluids)
12
Q
What are the two forms of T cell?
A
Helper T cells (TH cells)
Cytotoxic T cells (TC cells)
13
Q
What activates a T cell?
A
The binding of the T cell receptor to the antigen.
This is called cell-mediated immunity.
14
Q
Why are there millions of lymphocytes?
A
Each T lymphocyte responds to a different antigen.
15
Q
CELL-MEDIATED IMMUNITY - process
A
- Pathogens invade body cells or are taken in by phagocytosis.
- The phagocyte places antigens from the pathogen on the phagocytes cell surface membrane, so it becomes an antigen-presenting cell.
- Receptors on a specific T helper cell fit exactly onto these antigens.
- This attachment activates the T helper cell to divide rapidly by mitosis and form clones which are genetically identical to itself.
- These cloned cells have many uses such as activating cytotoxic T cells.
- These cytotoxic T cells are activated by the interaction with the clones and cytokines (which are produced by T helper cells).
- Once these cytotoxic cells are activated, they also divide by mitosis to produce cytotoxic T cell clones.
- Cytotoxic T cells produce a protein called perforin, which makes holes in the cell surface membrane of the infected host cell, resulting in cell death.
16
Q
CELL-MEDIATED IMMUNITY - what can the cloned T helper cells do?
A
- Develop into memory cells that enable a fast response to future infections by the same pathogen.
- Stimulate phagocytes to engulf pathogens by phagocytosis
- Stimulate B cells to divide, mature into plasma cells and secrete their antibodies - this goes into humoral immunity.
- Activate cytotoxic T cells.
17
Q
HUMORAL IMMUNITY - B-cells
A
- covered in antibodies, which will bind with complementary antigens.
- if an antigen ever enters the blood or tissue fluid, there will be a B cell with a complementary antibody to counter it.
- we have millions of B cells with different antibodies on them, present from birth, which multiply in response to an antigen.
- some develop into memory cells
18
Q
HUMORAL IMMUNITY - the process
A
- A specific T helper cell attaches to an antigen bound to an antibody on the surface of the B cell, which activates the B cell and causes it to divide.
- The B cell divides by mitosis, resulting in a clone of plasma cells (which are mature B cells which secrete antibodies). This process is known as clonal selection.
- These plasma cells become filled with ribosomes, ER and mitochondria - which allow the cells to produce large quantities of antibodies, as antibodies are proteins.
- The cloned plasma cells produce and secrete the specific antibody that binds to the antigen on the pathogens surface and destroys it.
- Finally, some of these B cells develop into memory cells.
19
Q
What are memory cells?
A
Cells that circulate in the blood and tissue fluid which can respond to future infections by the same pathogen to trigger a secondary response.
20
Q
Explain the primary immune response
A
- When an antigen enters the body for the first time, it activate the immune system, which is called a primary response.
- This response is slow as there aren’t many B-cells that can make the antibody needed to bind to the antigen.
- Eventually, the body will produce enough of the right antibody to overcome the infection. During this time, the infected person will develop symptoms of this disease.
- After being exposed to an antigen, both T and B cells produce memory cells.
- The memory cells remain in the body for a long time, and they remember the specific antigen so recognise the second time the antigen enters the body. Memory B cells record the specific antibodies needed to bind the antigen.
- The person is now immune - their immune system has the ability to respond quickly to a second infection.
21
Q
Explain the secondary immune response
A
- If the same pathogen reenters the body, the immune system will produce a quicker and stronger immune response - the secondary response.
- The process of 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 as well and divide into the correct type of T cells to kill the cell carrying the antigen.
- The secondary response often gets rid of the pathogen before you begin to show any symptoms - therefore you are immune to the pathogen.
22
Q
ANTIBODIES - What is an antibody?
A
An antibody is a protein produced by lymphocytes in response to the presence of an antigen.
23
Q
ANTIBODIES - variable regions
A
- this is what the specificity of an antibody relies on
- variable regions form antibody binding sites
- each antibody has a variable region with a unique tertiary structure (due to different primary sequences) which is complementary to one specific antigen
24
Q
ANTIBODIES - constant region
A
All antibodies have the same constant regions.
25
ANTIBODIES - look at picture of structure
26
ANTIBODIES - antigen-antibody complexes and their formation
- antigen-antibody complexes are formed when antibodies bind with antigens
- an antibody has two binding sites, and therefore, it can bind to two pathogens at once
27
ANTIBODIES - agglutination
- because antibodies can bind to two pathogen at the same time, pathogens become clumped together
- agglutinates bacteria attract the phagocytes, so they can phagocytose many pathogens at once
- once agglutinated, pathogens can’t do anything except wait to be engulfed and can’t do damage to the body
- the antibodies have “neutralised” the pathogen
28
MONOCLONAL ANTIBODIES - what are monoclonal antibodies?
Antibodies that are produced from a single clone (a group of genetically identical cells) of B cells.
This means they are identical in structure.
And because antibodies are very specific due to their unique tertiary structures, it is possible to make monoclonal antibodies that bind to anything (antigens, cells, etc).
29
MONOCLONAL ANTIBODES - creating them
1. Inject a mouse with the antigen you would like to create antibodies for.
2. Remove and extract B lymphocytes from the mouse.
3. Fuse B lymphocytes with a tumour cell (to increase speed of division) to create a hybridoma.
4. Screen for antibody production.
5. Allow it to divide by mitosis into clones.
6. Finally, isolate the monoclonal antibodies.
30
MONOCLONAL ANTIBODIES - treatment of cancer
- Cancer cells have antigens called tumour markers.
- You can make monoclonal antibodies that bind to these antigens.
- Anti-cancer drugs can be attached to the monoclonal antibodies.
- The drug will accumulate where there are cancer cells, so side effects will be lower.
31
MONOCLONAL ANTIBODIES - positive pregnancy tests
1. The application area contains antibodies for hCG bound to a blue bead.
2. When urine is applied, any hCG will bind to the antibody on the beads, forming an antigen-antibody complex.
3. The urine moves up the stick carrying any beads with it.
4. The test strip contains more antibodies to hCG and are immobilised.
5. Any hCG, with its blue beads attached, will bind to the immobilised antibodies.
6. Antibodies with blue beads but no hCG attach to the control strip to make sure the test worked.
32
MONOCLONAL ANTIBODIES - negative pregnancy tests
1. No hCG is present, so no antigen-antibody complexes formed (with antibodies attached to blue beads).
2. There is no hCG to bind to the immobilised antibodies, so no colour change occurs in the first line.
3. Antibodies with blue beads but no hCG attach to the control strip to make sure the test worked.
33
MONOCLONAL ANTIBODIES - ethical issues
- mice are used in the production of monoclonal antibodies. This could include deliberately inducing cancer in them.
- monoclonal antibodies have been used successfully to treat disease and save lives. However, some patients have died from their use in treatment of MS.
- testing new drugs can be dangerous - e.g. in 2006, six volunteers suffered multiple organ failure in a test
34
ELISA TEST - what does ELISA stand for?
Enzyme-linked immunosorbent assay
35
ELISA TEST - what is the function of the test?
- allows you to see if a patient has any antibodies to a certain antigen or any antigen to a certain antibody
- can be used to test for almost anything you can make an antibody for, including pathogenic infections and allergies
36
ELISA TEST - how does it work?
- an antibody that has an enzyme attached to it is used
- this enzyme can react with a substrate to produce a coloured product
- the colour change indicates the antigen or antibody is present, and the intensity of this colour indicates a quantity of antigen or antibody present.
37
ACTIVE AND PASSIVE IMMUNITY - natural active immunity
When you become immune after catching a disease.
38
ACTIVE AND PASSIVE IMMUNITY - artificial active immunity
A harmless dose of antigen in a vaccine produces memory cells against the pathogen.
39
ACTIVE AND PASSIVE IMMUNITY - natural passive immunity
For example, when a baby receives antibodies from its mother through the placenta or breast milk.
40
ACTIVE AND PASSIVE IMMUNITY - artificial passive immunity
When you are injected with antibodies such as anti-venom for a snake bite.
41
VACCINES - what do vaccines contain to trigger an immune response?
Antigens which are either free, or attached to a dead or attenuated (weakened) pathogen.
42
VACCINES - what happens when you are vaccinated?
- the antigens cause your body to produce memory cells against the pathogen, without the pathogen causing a disease
- you become immune without getting any symptoms
43
VACCINES - why are booster vaccines given?
To make sure that enough memory cells are produced.
44
VACCINES - how do you receive a vaccine?
- injection (this is what is usually on the mark scheme)
- orally - this could be broken down by the enzyme in the gut however or the molecules may be too large to absorbed into the blood
45
VACCINES - what is necessary for a vaccination programmes’ success?
- a suitable vaccines must be economically available in sufficient quantities to immunise those most vulnerable
- there must be few side effects otherwise people will be discouraged
- means of producing, storing and transporting vaccines
- means of administering at a suitable time - with trained staff and at different centres
- it must be possible to vaccinate the majority of a vulnerable population for herd immunity
46
VACCINES - what is herd immunity?
- herd immunity arrives when a sufficiently large proportion of the population has been vaccinated, making it difficult for a pathogen to spread within that population
- where the vast majority of the population is immune, it is unlikely that an unvaccinated individual will come into contact with an infected individual
- therefore, even those who aren’t immune are still protected
47
VACCINES - why do vaccines rarely actually eliminate disease?
- they aren’t always successful at producing immunity in an individual
- there could be many variations of the same pathogen, and not all of them have vaccines available - e.g. the cold virus is constantly evolving
- individuals could protest against pathogens for ethical, religious or medical reasons
- antigenic variability - some antigens are altered so memory cells don’t recognise and respond do them
48
What is antigenic variability?
- pathogens of a types of virus, bacteria, etc change their surface antigens due to mutations, so if you’re infected a second time, your memory cells don’t recognises the antigen, and the primary response takes place all over again, as you have no antibodies which are complementary to the antigen and bind to it.
- this causes problems when developing vaccines against certain pathogens like HIV and influenza
49
VACCINES - ethics
- developing vaccines often involves animals (e.g. animal testing)
- vaccines can have side effects that cause harm
- should vaccines be compulsory?
- who should vaccines be tested on?
- vaccines programmes are expensive and don’t always work. Could that money be used for treatment of other diseases?
50
HIV - what does HIV stand for?
Human immunodeficiency virus
51
HIV - what does AIDS stand for?
Acquired immune deficiency syndrome
52
HIV - what is a retrovirus?
A virus with the ability to make DNA from RNA due to the presence of reverse transcriptase.
53
HIV - structure
- **Lipid envelope** - made from membrane stolen from previous host cell
- **Core** - contains RNA and proteins, including the enzyme reverse transcriptase (which makes DNA from an RNA template, making HIV a retrovirus)
- **Capsid** - outer coat made of protein
- **Attachment proteins** - help HIV attach to a host cell (the T Helper cells)
LOOK AT PICTURE
54
HIV - life cycle of HIV
1. The attachment proteins attaches to receptor molecules on the cell-surface membrane of the T helper cell (the host cell).
2. The capsid is released into the cell, where it un-coats and releases the genetic material/RNA into the cell’s cytoplasm.
3. Inside the cell, the reverse transcriptase makes a complementary strand of DNA from the viral RNA template.
4. From this, double stranded DNA (from the viral RNA template) is made and inserted into the human DNA.
5. Host cell ribosomes and enzymes are used to make viral proteins from the viral DNA (by transcription and translation)
6. Viral proteins (e.g. capsid/protein coat) are assembled into new viruses, which bud from the cell and go on to infect the other cells.
55
HIV - how do we detect HIV?
When the immune system produces antibodies against the virus, these can be detected in the blood (e.g. with an ELISA test)
- therefore, a person who has anti-HIV antibodies is said to be HIV positive
56
HIV - how does HIV cause AIDS?
- people with HIV are classed as having AIDS when the number of T helper cells in their body reach a critically low level so that their immune system is no longer effective
- this may happen a few years after the initial infection (usually around 10 years)
57
HIV - what are symptoms of AIDS?
- many AIDS sufferers develop infections of the lungs, intestines, brain and eyes due to the bad performance of their immune system
- weight loss
- diarrhoea (and consequently dehydration)
- these infections, rather than HIV, is what ultimately causes death
58
HIV - control and treatment of HIV and AIDS
- currently their is no treatment for HIV
- antiretroviral drugs can slow down progression (basically manage the virus)
- HIV positive people can have almost as long a life expectancy as they would had they not been infected
59
HIV - how do retroviral drugs work?
They bind to the viral reverse transcriptase, preventing it from copying the viral RNA to make DNA.
60
Why are antibiotics ineffective against viruses?
- antibiotics work by destroying the bacterial cell **walls** or interfering with the metabolic pathways (the series of chemical reactions that occur within a cell)
- viruses are acellular, so they have no cell walls or metabolic pathway to act against
- viruses are also inside an organism’s cells, so antibiotics can’t reach them
61
Phagocytosis (mark scheme version)
1. Phagocyte attracted by a substance / recognises (foreign) antigen;
Accept named substance eg chemical / antigen
2. (Pathogen)engulfed / ingested;
Accept: description
3. Enclosed in vacuole / vesicle / phagosome;
4. (Vacuole) fuses / joins with lysosome;
5. Lysosome contains enzymes;
Accept named example of enzyme
6. Pathogen digested / molecules hydrolysed;
Neutral: Destroyed
62
What makes different antigens different?
Different tertiary structures.
63
What is a cytokine?
Chemicals that act as signalling molecules, including proteins and glycoproteins.
64
Explain viral replication
Viruses replicate by injecting their nucleic acid into a host cell.
1. First, a virus uses attachment proteins on its surface to bind to the complementary receptor proteins on the surface of a host cell.
2. The virus then injects its DNA or RNA into the host cell.
3. The host cell then uses its nucleus acid and protein building machinery (so ribosomes) to produce new viral particles.
65
Replication of HIV (mark scheme)
1. RNA converted into DNA using reverse transcriptase.
2. DNA inserted into T helper cell DNA.
3. DNA transcribed into HIV mRNA.
4. HIV mRNA translated into new HIV viral proteins for assembly into viral particles.
