1
Q
What happens as a B cell matures?
A
- As a B cell matures it gains the ability to make just one type of antibody moelcule
- While B cells are maturing, the genes that code for antibodies are changed in a variety of ways to code for different antibodies
- Each cell then divides to give a small number of cells that are able to make the same type of antibody
- Each small group of identical cells is called a clone
2
Q
What happens after a clone is formed?
A
- At this stage the antibody molecules do not leave the B cell but remain in the cell surface membrane, here, part of each antibody forms a glycoprotein receptor, which can combine specifically with one type of antigen
- If that antigen enters the body, there will be some mature B cells with cell surface receptors that will recognise it
3
Q
What happens when the antigen enters the body?
A
- When the antigen enters the body for the first time the small numbers of B cells with receptors complementary to the antigen are stimulated to divide by mitosis
- This stage is known as clonal section
- The small clone of cells divides repeatedly by mitosis in the clonal expansion stage so that high numbers of identical B cells are produced over a few weeks
4
Q
What are plasma cells?
A
- Some of these activated B cells become plasma cells that produce antibody molecules very quickly, up to several thousand a second
- Plasma cells secrete antibodies into the blood, lymph or onto the lines of the lungs and the gut
- These plasma cells do not live long; after several weeks their numbers decrease
- The antibody molecules they have secreted stay in the blood for longer, however until they too eventually decrease in concentration
5
Q
What are memory cells?
A
- Other B cells become memory cells
- These cells remain circulating in the body for a long time
- If the same antigen is reintroduced a few weeks or months after the first infection, memory cells divide rapidly and develop into plasmas cells and more memory cells
- This is repeated in every subsequent invasion by the same antigen, meaning that the infection can be destroyed and removed before any symptoms of the disease develop
6
Q
What is the primary and secondary response?
A
- The primary response is slow because, at this stage there are very few B cells that are specific to the antigen
- During the primary response the number of cells in each clone of B cells that is selected has increased in size. There are many more B cells specific to the pathogen that has invaded the body. Many more antibodies are produced in the secondary response - The secondary response is faster because there are now more memory cells, which quickly divide and differentiate into plasma
7
Q
What is your immunological memory?
A
- Memory cells are the basis of immunological memory; they last for many years, often a lifetime (this explains why someone is very unlikely to catch measles twice)
- There is only one strain of the virus that causes measles, and each time it infects the body there is a fast secondary response
- However repeated infections of the common cold and influenza, because there are many different new strains of the viruses that cause these diseases, each one having different antigens
- Each time a pathogen with different antigens infects us, the primary response emus occur before we become immune, and during that tine we often become ill
8
Q
What are T-lymphocytes?
A
- Mature T-cells have specific cell surface receptors called T cell receptors
- T cell receptors have a structure similar to that of antibodies and they are each specific to one antigen
9
Q
What is antigen presentation?
A
- T-cells are activated when they encounter this antigen on another cell of the host (that is, on the person’s owns cells)
- Sometimes this cell is a macrophage that has engulfed a pathogen and cut it up to expose the pathogen’s surface molecules, or it may be a body cell that has been invaded by a pathogen and is similarly displaying the antigen on its cell surface membrane as a kind of ‘help’ signal
- The display of antigens on the surface of cells in this way is known as antigen presentation
- Those T-cells that have receptors complementary to the antigen respond by dividing by mitosis to increase the number of cells
- T cells go though the same stages of clonal selection and clonal expansion as clones of B cells
10
Q
What are the two main types of T cell?
A
- Helper T cells
2. Killer T cells (or cytoxic T cells)
11
Q
What happens when helper T cells are activated?
A
- They release hormone-like cytokines that stimulate appropriate B cells to divide, develop into plasma cells and secrete antibodies
- Some T helper cells secrete cytokines that stimulate macrophages to carry out phagocytosis more vigorously
12
Q
What do killer T cells do?
A
- Killer T cells search the body for cells that have become invaded by pathogen and are displaying foreign antigens from the pathogen on their cell surface membranes
- Killer T cells recognise the antigens, attach themselves to the surface of infected cells, and secrete toxic substance such as hydrogen peroxide, killing the body cells and the pathogens inside
13
Q
What is another role of helper T cells? What are memory cells in T cells like?
A
- Some helper T cells secrete cytokines that stimulate macrophages to carry out phagocytosis more vigorously, or that stimulate killer T cells to divide by mitosis and to differentiate by producing vacuoles full of toxins
- Memory helper T cells and memory killer T cells are produced, which remains in the body and become active very quickly during the secondary response to antigens
14
Q
What are antibodies?
A
- Antibodies are globular glycoproteins with quaternary structure
- They form a group of pals proteins called immunoglobulins
15
Q
What is the basic molecule of antibodies like?
A
- The basic molecule common to all antibodies consists of four polypeptide chains: two “long” or “heavy” chains and two “short” or “light” chains
- Disulphide bonds hold the long/heavy chains together
- Each molecule has two identical antigen-binding sites, which are formed by both light and heavy chains
- The sequence of amino acids in these regions make the specific 3D shape which bonds to just one type of antigen
16
Q
What is the variable region of an antibody?
A
- The antigen-binding sites form the variable region, which is different on each type of antibody molecule produced (specific)
- The ‘hinge’ region gives the flexibility for the antibody molecule to bind around the antigen
17
Q
What are the different types of phagocytes? Where are they produced?
A
- Phagocytes are produced throughout the life in the bone marrow and they are stored there before being distributed around the body in the blood
- Neutrophils, macrophages and monocytes
- Phagocytes have their origin in the bone marrow
18
Q
What are neutrophils?
A
- They from about 60% of the white blood cells in the blood
- They travel throughout the body, often leaving the blood through the walls of capillaries to ‘patrol’ the tissues
- During infection neutrophils are released in large numbers from their stores, but they are short-lived cells
19
Q
What are macrophages?
A
- They are larger than neutrophils and tend to be found in organs such as the lungs, liver, spleen kidneys and lymph node, rather than remaining in the blood
- After they are made in the bone marrow macrogphages travel in the blood as MONOCYTES, which develop into macrophages as they leave the blood and settle in the organ, removing any foreign matter found there
- Macphages are long-lived cells and play a crucial role in initiating the immune response, since they do not destroy pathogens completely, but cut them up to display antigens that can be recognised by lymphocytes
20
Q
Describe the stages of phagocytosis
A
- Attraction (chemotaxis)
- Recognition and attachment
- Endocytosis
- Bacteria within a phagocytic vacuole
- Fusion of lysosomes and phagocytic vacuole
- Killing and digestion
21
Q
What happens during phagocytosis?
A
- If pathogens invade the body and cause an infection, some of the cells under attack respond by releasing chemicals such as histamine
- These, with any chemicals released by the pathogens themselves, attract passing neutrophils to the site and this movement towards a chemical stimulus is called chemotaxis
- The neutorphils destroy the pathogens by phagocytosis
22
Q
How do neutrophils act in phagocytosis?
A
- The neutrophils move toward the pathogen, which may be clustered together and covered in antibodies
- The antibodies further stimulate the neutorphils to attack the pathogens
- This is because neutrophils have receptor proteins on their surfaces that recognise antibody molecules and attach to them
- When the neutrophil attaches to the pathogen, the neutrophil’s cell surface membrane engulfs the pathogen and traps it within a phagocytic vacuole, in a process called endocytosis
- Digestive enzymes are secreted into the pahgocytic vacuole, so destroying the pathogen
- Neutrophils have a short life: after killing and digesting some pathogens, they die. Dead neutorphils often collect at a site of infection to form pus
23
Q
What is an antigen?
A
An antigen is a substance that is foreign to the body and stimulates and immune response
24
Q
What is an antibody?
A
An antibody is a glycoprotein (immunoglobulin) made by plasma cells derived from B-lymphocytes, secreted in response to an antigen; the variable region of the antibody molecule is complimentary in shape to its specific antigen
25
What is the immune response?
The immune response is the complex series of responses of the body to the entry of a foreign antigen; it involves the activity of lymphocytes and phagocytes
26
What is non-self?
Non-self refers to any substance or cell that is recognised by the immune system as being foreign and will stimulate an immune response
27
What is self?
Self refers to substances produced by the body that the immune system does not recognise as foreign, so they do not stimulate an immune response
28
What are the two types of white blood cells?
1. Lymphocytes
| 2. Phagocytes (e.g. neutrophils and macrophages)
29
When do the number of white blood cells increase in the body?
1. The number of neutrophils in the blood increases during bacterial infections and whenever tissues become inflamed and die
2. The number of lymphocytes in the blood increases in viral infections and in TB
3. Most of the lymphocytes that circulate in the blood are T cells
30
Where do the white blood cells originate from?
1. Myeloid Stem cells in the bone marrow, give rise to monocytes, neutrophils and platelets
2. Lymphoid Stem cells in the bone marrow give rise to lymphocytes, both B and T cells
31
What happens in Leukemias?
1. Leukemias are cancers to these stem cells, and the cells divide uncontrollably to give many cells which do not differentiate properly and disrupt the production of normal blood cells including rbcs and platelets
2. These malignant cells full up the bone marrow and then flow into the blood and into the lymphatic system
32
What are the different types of leukaemia?
1. In myeloid leukaemia, the stem cells responsible for producing neutrophils divide uncontrollably and the number of immature cells increases
2. In lymphoblastic leukeamias, the cancerous cells are those that give rise to lymphocytes
33
What is the affect of leukaemia on the body?
1. The immature white blood cells are produced very quickly and they disrupt the normal balance of components in the blood
2. This means that the body does not have enough red blood cells or platelets
3. This causes anaemia and increases the risk of excessive bleeding
4. Also, the number of mature neutrophils and lymphocytes decrease so that people with these cancers become more susceptible to infections; they are said to be immunosuppressed
34
What are the different forms of leukaemia?
- There are acute and chronic forms of both types of leukaemia
1. Acute Leukemias develop very quickly, have severe effects and need to be treated immediately after being diagnosed
2. Chronic leukemias may take many years to develop and changes in blood cell counts are usually monitored over time so that treatment is given when it is most likely to cure the disease
3. Blood tests are used to help diagnose these diseases, monitor their progress and asses the effectiveness of treatments
35
What is active immunity?
Active immunity is gained when an antigen enters the body, an immune response occur and antibodies are produced by plasma cells
36
What is passive immunity?
Passive immunity is immunity gained without an immune response; antibodies are injected (artificial) or pass from mother to child across the placenta or in breast milk (natural)
37
What is natural immunity?
Natural immunity is gained by being infected (active) or by receiving antibodies from the mother across the placenta or in breast milk (passive)
38
What is artificial immunity?
Artificial immunity is immunity gained either by vaccination (active) or by injecting antibodies (passive)
39
What is vaccination?
Vaccination is giving a vaccine contains antigens for a disease, either by injection or by mouth; vaccination confers artificial active immunity
40
How can vaccination control disease?
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41
Why was the eradication of smallpox successful? 1
1. The various virus was stable, it did not mutate and change its surface antigens
- This meant that the same vaccine could be used everywhere in the world through the campaign and it was therefore cheap to produce
2. The vaccine was made from a harmless strain of a similar virus (vaccinia) and was effective because it was a 'live' vaccine
3. The vaccine was freeze-dried and could be kept at high temperatures for as long as six months
- This made it suitable for use in the tropics
4. Infected people were easy to identify
42
Why was the eradication of smallpox successful? 2
1. The vaccine was easy to administer and was even more effective after the development of a stainless steel, reusable needle for its delivery. This 'bifurcated' needle' had two prongs, which were used to push the vaccine into the skin
2. The smallpox virus did not linger in the body after an infective to become active later and form a reservoir for infection
3. The virus did not infect animals, which made it easier to break the transmission cycle
4. Many 16- to 17-year-olds became enthusiastic vaccinator and suppliers of information both cases; this was especially valuable in remote areas
43
Why is it hard to make eradication successful?
1. Unstable political situation
2. Public health facilities are difficult to organise in developing countries with poor infrastructure
3. Few trained personnel and limited financial resources
4. They are almost impossible to maintain during period of civil unrest or during a war
44
Why is preventing measles hard?
1. Measles is a preventable disease and one that could be eradicated by a worldwide surveillance and vaccination programme
2. However a programme of one-does vaccination has not eliminated the disease in any country, despite high converge of the population
3. This is explained by the poor response to the vaccine shown by some children who need several boosters to develop full immunity
4. In large cities with high birth rates and shifting populations, it can be difficult to give boosters, following up cases of measles and trace contacts
5. Migrants and refugees can from reservoirs of infection, experiencing epidemics within their communities and spreading the disease to surrounding populations
6. This makes measles a very difficult disease to eradicate, even with high vaccination coverage
45
What is the estimated herd immunity needed for measles?
93%-95%
46
What so the constant region on an antibody molecule?
Binds to receptors of phagocytes and marked them for phagocytosis
47
Why can viruses not be treated with antibiotics?
1. Antibiotics are not effective against HIV viruses
2. Viruses have no sites where antibiotic can work
3. Viruses have no cell wall
4. Viruses are within cells and so antibiotics cannot reach them
48
What are autoimmune diseases?
A type of disease in which there is a mistaken immune response to a self antigen leading to the production of antibodies and the destruction of body tissues; myasthenia gravis is an example
49
Why do autoimmune diseases occur?
1. The immune system attacks one or more self antigens, usually proteins
2. During the maturation of T cells in the thymus, many cells are destroyed as T cells receptors that are complementary to self antigens
3. Some of these T cells evade destruction and sometime activated to stimulate an immune response agains the body's own proteins
4. This starts an attack often involving antibodies and killer T cells against parts of the body
- In some autoimmune diseases, the attack is located and directed against one organ and in others it is directed agains the whole body
50
What is myasthenia gravis (MG)? How do motor neurones work?
- An autoimmune disease that targets the neuromuscular junctions between motor neurones and skeletal muscle cells
1. Motor neutrons transit nerve impulses to muscle cells and where they terminate they release acetylcholine, a cell signalling molecule into small gaps between muscle fibres and neurons
2. Ach binds with rector proteins on CSM of muscle fibres and this stimulates opening of channels so that sodium ions move through the membrane leading to depolarisation
51
What is different for people with MG?
1. They have helper T cells specified for the CS receptors for acetylcholine
2. Under certain conditions these stimulate a clone of B cells to differentiate into plasma cells and secrete antibodies that bind to the respecter so blocking the transmission of impulses from motor neurones
3. Muscle fibres absorb the reactor antibody complex and destroy them
4. Without acetylcholine receptors, muscles cells do not recite ay stimulation and because muscles are not stimulated the muscle tissue begins to break down
52
What are the symptoms of MG?
- Muscle weakness that gets worse with activity and improves with rest
- Affected muscle become fatigued very easily
53
What are some treatments for MG?
1. Drug that inhibits the enzyme in synapses that breaks down acetylcholine and so increase the concentration of acetylcholine in synapses so its action in stimulating muscle fibres to contract last longer
2. Surgical removal of the thymus gland, as it is the site of the helper T cells thats stimulate B cells to produce antibodies to the acetylcholine receptors
54
What are other autoimmune diseases?
1. Multiple sclerosis, nerve cells in brain and spinal cord loose myelin sheath that surround them, degenerating areas (plaques) detected using MRI. Loss of protective myelin, stop conation impulses and loss of function controlled by areas of CNS concerned. Symptoms of muscle weakness, loss of sensory input from the skin, poor vision
2. Rheumatoid arthritis: long term destructive process sin joints initially finger and hand joint then to shoulders, tendons becomes inflamed and constant muscle spams and pain, so people find hard to keep mobile
3. Type 1 inulin dependent diabetes, partly cause by virus infection making cell that secrete insulin in rho pancreas unrecognisable as seed. Killer T cells enter the islets of Langerhans and destroy the cells that produce insulin
55
What are the cause of autoimmune diseases?
- MG not inherited condition
- People with certain alleles of genes involved in cell recognition are at higher risk of developing MG that those without these alleles
- Genetic factors involved as it has been shown that susceptibly to the diseases is inherited
- Environmental factors also important
56
How do you manufacture antibodies on a large scale?
- A very large number of cells of a particular B cell clone, all secreting identical or monoclonal antibodies (Mabs)
- Problem is that B cells divide by mitosis do not produce antibodies and plasma cells that secrete antibodies do not divide
- So use cell fusion
57
What is cell fusion?
1. A small number of plasma cells producing a particular antibody fused with cancer cells
2. Cancer cells go on dividing indefinently
3. The cell produced by this fusion of a splay cell and a cancer cells is called a hybridoma
4. Hybridoma cells divide by mitosis and secrete antibodies
58
How can you use monoclonal antibodies in diagnosis?
1. Used to locate position of blood clots in body of a person though to have deep vein thrombosis
2. The antibodies are produced by injecting a mouse with human fibrin the main protein found in blood clots
3. The mouse makes many plasma cell that secrete the antibody against fibrin and these plasma cells are collected from its spleen
4. The plasma cells are used with cancer cells to form hybridomas that secrete the antifibrin antibody
5. A radioactive chemical that produces gamma radiation is attached to each antibody molecule to make radioactively labelled antibodies
59
What happens once the labelled antibodies are introduced into the patients blood?
1. As the Maps are carried around the body in the bloodstream, they bind to any fibrin molecules with which they come into contact
2. The radioactivity emitted by these labelled antibodies is used to detect where they are in the body
3. A gamma-ray camera is used to detect the exact position of the antibodies in the person's body
4. The position of the labelled Maps indicates the position of any blood clots
60
What are other diagnosis using Mabs?
- Mabs can locate cancer cells, which have proteins on their CSM that differ rom the proteins on normal body cells and can therefore be detected by antibodies
- Can identify exact strain of a virus or bacterium causing an infection, speeds up choice of treatment
- Used routinely in blood typing before transfusion and tissue typing before transplant
61
Summarise how monoclonal antibodies are produced
1. Antigen injected
2. Mouse B cells that recognise the antigen proliferate and form plasma cells
3. Cell fusion
4. Tiny samples are taken so that there is only one cell present in a well. Every well is tested so that any hybridoma cells that produce the required antibody can be found
5. A clone of cells is produced which only makes this one antibody
- Mabs have many different uses in research and in medicine, both in diagnosis and treatment
62
What is different with Mabs for treatment or diagnosis?
1. When monoclonal antibodies are used in diagnosis, usually administered once
2. Used as treatment need to be administered more than once, and this is a problem as antibodies are produced by laboratory animals and so when introduced into humans they trigger an immune response because they are foreign (non-self)
63
How have they humanised Mabs?
1. Altering the genes that code for the heavy and light polypeptide chains of the antibodies so that they code for human sequences of amino acids, rather than mouse or rabbit sequences
2. Changing the type and position of the surf groups that are attached to the heavy chains to the arrangement found in human antibodies
64
Which Mabs have been used to treat what?
1. Trastuzumab used in treatment of some breast cancers, humanised mouse monoclonal antibody and binds to a receptor protein that is produced in abnormal quantities in the CSM of some breast cancers
2. The receptor protein is not unique to cancer cells, but cells with between 10 and 100 time she usual number of these receptor molecules in their CSMs can only be cancer cells
3. Trastuzumab binds to these cells and this makes them out for destruction by the immune system
65
What is Ipilimumab?
- More recent cancer therapy for melanoma
- Works by activating the immune system, by binding to. protein produced buy T cells, the role of which is to reduce the immune response
- By closing the action of the protein an immune response can be maintained against the cancer cells
66
What is the Influxumab Mab?
1. Used to treat rheumatoid arthritis
2. Binds to proteins secreted by T cells that causes damage to the cartilage in joint and blocks its action
3. Most of those treated for rheumatoid arthritis receive this therapy at monthly or two monthly intervals, so important Mab is humanised and does not itself trigger an immune response
67
What is the Rituximab Mab?
- Control B lymphocytes
- Binds to cell surface membrane receptor protein found on the surface of B cells, but not on the surface of plasma cells
- After bringing to B cells this Mab causes a variety of changes that lead tot he death of the cell
- This Mab used to treat diseases in which there is an overproduction or inappropriate production of B cells, such as leukuamias and autoimmune diseases
- Reducing the number of B cells appears to reduce severity of deceases, such as multiple sclerosis and rheumatoid arthritis this Mab also trialled successfully of myasthenia gravis
68
What is hybridoma?
A cell formed by the fusion of a plasma cell and a cancer cell; it can both secrete antibodies and divide to form other cells like itself
69
What are monoclonal antibodies?
Many identical antibodies, made by hybridoma cells formed by the fusion of a plasma cell and a cancer cell
70
Where do phagocytes (macrophages and neutrophils) have their origin?
Bone marrow
71
When would there be an increased level of white blood cells?
-Humans with infectious diseases and leukaemia
72
Why is it important that many identical plasma cells are produced?
- Part of immune response
- Produce increase concentration of antibody
- Therefore more effective against pathogen
- Specific antigen
- Antibody produced are the same
73
Outline the hybridoma method for the production of a monoclonal antibody
1. Mouse is injected with an antigen
2. Wait for immune response to occur
3. Clonal selection
4. Clonal expansion
5. Plasma cells extracted
6. From mouses's spleen
7. Fused with cancer cells
8. Hybridoma cells formed
9. Hybridoma cells reducing antibodies identified
10. Cultured on a large scale (to secrete monoclonal antibodies)
74
What is the function of the constant region?
Bind to receptors on phagocytes / antigen marking for phagocytosis
75
Explain how the tertiary structure of a protein results in it being globular
1. Coiling/folding to form tertiary structure
2. Interactions of R groups such as ionic/hydrogen/hydrophobic
3. Hydrophobic R groups on insides and amino acids with hydrophilic R groups face outwards
76
What is the variable region?
Bind to antigen specific
77
What do disulphide bonds do?
Holds polypeptides together/maintains tertiary structure
Z A level Biology
flashcards
Decks in class (15)
# Cards
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The Cell70
-
Gas Exchange And Smoking25
-
Biological Molecules63
-
Cell Membranes and Transport55
-
Microscope0
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Biological Molecules COPY19
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Transport in Mammals56
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Immunity77
-
Infectious Diseases68
-
Genetic Technology3
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Transport in plants74
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Transport in plants 259
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Energy and Respiration133
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Biodiversity, classification and conservation89
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Experiments A210
