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A level- Biology COPY > The specific immune response and immunity > Flashcards

The specific immune response and immunity Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

Define the term “antigen” and differentiate between “self” and “non-self” antigens.

A

Identifying chemical on the surface of the cell that triggers an immune response.
Self antigens are on your own cells and non-self antigens are on the cells of pathogens

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2
Q

Define the term antibody

A

Y-shaped glycoproteins made by B ells of the immune system in response to the presence of an antigen

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3
Q

Define the term antigen-antibody complex

A

The complex formed when an antibody binds to an antigen

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4
Q

Define the term lymphocyte

A

WBC that make up the specific immune response

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5
Q

Define the term specific immune response

A

It is the slower than non-specific responses.

However the immune memory cells mean it reacts very quickly to a second invasion by the same pathogen

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6
Q

Draw, label and annotate a diagram of an antibody.

A
  1. Y-shaped- made up of two identical long polypeptide chains called the heavy chains and two much shorter chains called the light chains
  2. The chains are held together by disulfide brides as well as disulfide bridges within the polypeptide chain holding them in shape
  3. Bottom of y is receptor binding site
  4. Two ends of the branches of the y are the antigen binding sites- variable region - is a different shpa eon each antibody- gives it it’s specificity
  5. the rest is the constant region and is always the same
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7
Q

Describe and explain 4 ways in which antibodies defend the body.

A
  1. The antibody of the antigen-antibody complex acts as an opsonin so the complex is easily engulfed and digested by phagocytes
  2. Most pathogens can no longer effectively invade the host cells once they are part of an antigen-antibody complex.
  3. Antibodies act as agglutinins causing pathogen carrying antigen-antibody complexes to clump together. This helps to prevent them form spreading through the body- makes it easier for phagocytes to engulf a number of pathogens at the same time
  4. Antibodies act as anti-toxins, binding to the toxins produced by pathogens and making them harmless
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8
Q

Explain why B lymphocytes are called “B” whereas T lymphocytes are called “T”.

A
  1. B lymphocytes mature in the Bone marrow

2. T lymphocytes mature in the Thymus gland

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9
Q

Name the 4 main types of T lymphocytes

A
  1. T helper cells
  2. T killer cells
  3. T memory cells
  4. T regulator cells
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10
Q

Decribe the role of T helper cells

A
  1. Have receptors on their cell-surface membrane which bind to the surface antigens on APCs
  2. Produce interleukins- type of cytokine (cell signalling molecule)
  3. These interleukins help to stimulate the activity of B cells which increases antibody production, stimulates the production of other types of T cells and attracts and stimulates macrophages to ingest pathogens with antigen-antibody complexes
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11
Q

Describe the role of T killer cells

A
  1. Destroy pathogens carrying the antigen
  2. Produce a chemical called perforin which kills the pathogen by making holes in the cell membrane so it is freely permeable
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12
Q

Describe the role of T memory cells

A
  1. Live for long time as part of immunological memory
  2. If they meet an antigen for the second time they divide rapidly to form a huge number of clones of T killer cells that destroy the pathogen
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13
Q

Describe the role of T regulator cells

A
  1. Suppress the immune system acting to control and regulate it.
  2. They stop the immune response once a pathogen has been eliminated and make sure the body recognises self antigens and does not set up an autoimmune response
  3. Interleukins are important in this control
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14
Q

Name the 3 main types of B lymphocytes

A
  1. Plasma cells
  2. B effector cells
  3. B Memory cells
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15
Q

Describe the role of plasma cells

A
  1. Produce antibodies to a particular antigen and release them into the circulation
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16
Q

Describe the role of B effector cells

A
  1. Divide to form plasma cell clones
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17
Q

Describe the role of B memory cells

A
  1. Live a long time as part of the immunological memory
  2. Programmed to remember a specific antigen and enable the body to make a very rapid response when a pathogen carrying that antigen is encountered again
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18
Q

Define the term “cell mediated immunity” and suggest what it is particularly effective against.

A
  1. T lymphocytes respond to cells of an organism that have been changed in some way e.g. by a virus infection, by antigen processing or by mutation (cancer cell) and to cells from transplanted tissue
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19
Q

Describe the process of cell mediated immunity.

A
  1. Antigen presenting cells formed:- from phagocytosis, a viral infection or cancer
  2. APC comes into contact with many different T helper cells – only T helper cells with complementary receptors to the antigens will be activated.- Clonal selection
  3. T helper cells produce interleukins which stimulate other types of activated T-cell to clone by mitosis (as well as making the T helper cells themselves clone by mitosis)- Clonal expansion
  4. T cells cloned may:
    - develop into T memory cells which give a rapid response if this pathogen invades again
    - Develop into T helper cells which either produce interleukins that stimulate phagocytosis or produce interleukins that stimulate B cells to clone by mitosis
    - Stimulate the development of a T killer cells that are specific for the presented antigen and then destroy infected cells
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20
Q

Define the term “humoral immunity” and suggest what it is particularly effective against.

A
  1. The body responds to antigens found outside the cells- bacteria, fungi and to APCs.
  2. The humoral immune system produces antibodies that are soluble in the blood and tissue fluid and are not attached to the cells.
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21
Q

Describe the process of humoral immunity.

A
  1. B lymphocytes have antibodies on their cell surface membrane which are specific to only one antigen,
  2. When a pathogen enters the body, a B cell with complementary antibodies will bind to the antigens on the pathogen - it will engulf and process the antigen to become an APC.
  3. Clonal selection- Selection of the appropriate B cell by the T helper cells to be cloned- T cell binds to the B cell APC
  4. Clonal expansion- T helper cell produces interleukins to activate the B cells which then divide by mitosis to produce clones
  5. B cells differentiate to form plasma and B effector cells and B memoery cells
  6. Plasma cells secrete antibodies which are specific to the antigen which help to destroy the pathogen
  7. Memory cells remain in circulation to provide a secondary response- faster response to subsequent exposure
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22
Q

Define the term primary immune response

A

The relatively slow production of a small number of the correct antibodies the first time a pathogen is encountered

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23
Q

Define secondary immune response

A

The relatively fast production of very large quantities of the correct antibodies the second time a pathogen is encountered as a result of the immunological memory.

24
Q

Draw, label and annotate a graph of quantity of antibody in the blood over time to compare the primary and secondary immune responses.

A
  1. Secondary immune response produces a lot more anitbodies
  2. The rate at which antibodies are produced is much faster
  3. They are quicker to start producing antibodies
25
Q

Why is the secondary immune response quicker

A
  1. Antigen presentation still happens
  2. Clonal selection- many more cells
  3. Clonal expansion- less needs to happen because there are already a lot of cells- memory cells- this is what saves the most time
26
Q

Define active immunity

A

The type of immunity you get when your immune system makes its own antibodies after being stimulated by an antigen.

27
Q

Define passive immunity

A

Type of immunity when you are given antibodies made by a different organism

28
Q

Define natural immunity

A

Occurs when the person is exposed to a live pathogen develops the disease and becomes immune as a result of the primary immune response- developed without intervention

29
Q

Define artificial immunity

A

Body is given immunity to a disease by intentional exposure to small quantities of it

30
Q

Give one example for each of natural active immunity, natural passive immunity, artificial active immunity and artificial passive immunity.

A

Natural active- immune after catching a disease
Natural passive- baby becomes immune due to antibodies it receives form its mother though placenta/ breast milt
Artificial active- Vaccination
Artificial passive- Injected with antibodies from someone else

31
Q

Draw a table comparing active and passive immunity.

A

Time taken- A: not immediate, P: immediate
Duration- A: long term, P: short term
Exposure to antigens- A: Yes P: No
Clonal expansion/selection- A: Yes, P:No
Antibodies supplied/ made- A: made, P: supplied
Production of memory cells- A: yes, P: no
Requires fully functioning immune system- A: Yes, P: no

32
Q

Define the term “autoimmune disease” and name and describe 3 examples of autoimmune diseases.

A

Autoimmune disease- a condition or illness resulting from an autoimmune response- when the immune system acts against its own cells and destroys health tissue in the body

  1. Lupus- immune system attacks cells in connective tissue which causes painful inflammation- affects skin, joints and heart and lungs
  2. Rheumatoid arthritis- attacking cells in the joints which cases pain and inflammation
  3. Type 1 diabetes- affects insulin-secreting cells of the pancreas
33
Q

Suggest how autoimmune diseases may occur.

A

If the immune system can’t recognise self antigens so treats them as foreign antigens and launches an immune response against organisms own tissues

34
Q

Define vaccine

A

A safe form of an antigen which is injected into the blood stream to provide artificial active immunity against a pathogen bearing the antigen

35
Q

Define vaccination

A

The administering of a vaccine causing immunisation

36
Q

Describe 5 ways in which antigens can be obtained for use in vaccines.

A
  1. Isolated antigens
  2. Genetically engineered antigens
  3. Killed or inactive pathogens
  4. Weakened (attenuated) pathogens
  5. Altered toxins
37
Q

Describe how vaccination results in artificial active immunity.

A
  1. It triggers the primary immune response by the foreign antigens and your body produces antibodies and memory cells
  2. If you come into contact with a live pathogen, the secondary immune response is triggered and you destroy the pathogen rapidly
38
Q

Define the term epidemic

A

When a communicable disease spreads rapidly to a lot of people at a local or national level

39
Q

Define the term pandemic

A

When a communicable disease spreads rapidly to a lot of people across a number of countries

40
Q

Define the term “herd immunity”.

A

When a significant number of people have been vaccinated, this gives protection to those who do not have immunity - herd immunity - as there is minimal opportunity for an outbreak to occur.
Helps people who can’t get vaccinated- young, old or immunosupressed people

41
Q

Give two examples of vaccination programmes that aim to provide herd immunity.

A
  1. MMR- given to children at a year old and just before they start school
  2. Meningitis C - given to babies at 3 months and boosters are given at 1 year and to teens.
42
Q

Suggest why the Influenza vaccine needs to be redeveloped and people need to be revaccinated each year.

A
  1. Because the antigens on the surface of the influenza virus change regularly forming new strains of the virus
  2. Memory cells produced from the vaccination with one strain of the flu will not recognise other strains with different antigens- immunologically different
43
Q

Describe 6 examples of common medicinal drugs derived from living organisms.

A
  1. Penicillin- from mould on melons- antibiotic
  2. Docetaxel- derived from yew trees- treatment for breast cancer
  3. Aspirin- based on compounds from sallow bark- painkiller, anti-coagulent, anti-pyretic, anti-inglammatory
  4. Prialt- derived from venom of a cone snail- pain killing drug
  5. Vancomycin- derived from soil fungus- one of most powerful anti-biotics
  6. Digoxin- based on digitoxin originally extracted from foxgloves- powerful heart drug used for atrial fibrillation and heart faliure
44
Q

Explain the need to maintain biodiversity in relation to the discovery of new medicines.

A

If we don’t protect biodiversity some species may die out before we get a chance to study them.
They could prove to be useful sources of medicine

45
Q

Define the term “personalised medicine”, give an example of how treatment is being personalised, and suggest the value of personalising medicine to a person’s genetic information.

A
  1. They are medicines that are tailored to an individual’s DNA- dependent upon the characteristics of the individual (size, age but particularly the individual’s genomes)
  2. The theory is that doctors will be able to predict how you will respond to different drugs and only prescribe the ones that will be most effective for you- avoid side effects.
46
Q

Define the term “synthetic biology” and give 2 examples of how synthetic biology may lead to better medical treatments.

A
  1. Involves using technology to design and make things like artificial proteins, cells and even microorganisms.
  2. scientists are looking at engineering bacteria to destroy cancer cells while leaving healthy body cells intact
  3. Drugs produced by organisms that wouldn’t normally make that chemical- genetic engineering
47
Q

Define the term antibiotic

A

A chemical or compound that kills or inhibits the growth of bacteria

48
Q

Define the term selective toxicity

A

The ability to interfere with the metabolism of a pathogen without affecting the cells of the host.

49
Q

Draw a table to outline the different ways 4 common antibiotics have their effect.

A
  1. Affects cell walls made of peptidoglycan- burst
  2. Enzymes- inhibit the metabolic pathways
  3. Bacteria have a circular chromosome that is different to humans, so they can target the different DNA replication- prevent reproduction
  4. Ribosomes- prevent protein synthesis
  5. Make holes in the membrane altering the permeability
50
Q

Explain why antibiotics do not work on viral infections.

A
  1. Target things only bacteria have

2. Viruses use our system to reproduce to stop they would kill our cell as well

51
Q

Explain how a population of bacteria may develop resistance to an antibiotic.

A
  1. You start with a population with no resistance o bacteria
  2. A chance mutation in one bacterium produced a gene for antibiotic resistance- creating a population with a few antibiotic resistance bacteria
  3. Antibiotic A applies a selection pressure- there is a strong natural selection for bacteria with a gene for antibiotic-resistance
  4. This creates a population with mainly antibiotic-resistance
  5. Continued selection pressure means almost all bacteria on the population will be antibiotic resistant
52
Q

Suggest two ways in which the use of antibiotics may be increasing the likelihood of resistance evolving.

A
  1. Farmers using antibiotics in animal feed to prevent animals losing condition due to infection
  2. Over subscription to antibiotics
53
Q

Give two examples of antibiotic resistant bacteria.

A

MRSA, C.difficile

54
Q

Suggest two methods used to reduce the likelihood of resistance developing in bacteria.

A
  1. Minimising he use of antibiotics and ensuring every course of antibiotics is completed- reduces risk of resistant individuals surviving and developing into a resistant strain population
  2. Good hygiene in hospitals, care home and in general- major impact on spread of all infections
55
Q

Explain why not completing a course of antibiotics may lead to antibiotic resistance developing.

A
  1. Only weaker bacteria will be killed if you don’t finish it which allows stronger bacteria to become resistant

A level- Biology COPY (46 decks)

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