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AS AQA Biology > Immunology > Flashcards

Flashcards in Immunology Deck (75)
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1
Q

Define infection

A

An interaction between a pathogen and a hosts defence mechanisms

2
Q

Define imunity

A

An infection won’t occur a second time

3
Q

Define antigen

A

A molecule that indices an immune response

4
Q

Define antibody

A

It is a complex quaternary protein (it has two heavy chains and two light chains) which is produced and secreted by plasma B cells. Each antibody has 2 identical binding sites called variable regions which are specific to one antigen, meaning the can bind together forming an antibody-antigen complex.

5
Q

What are the first defence mechanisms preventing infection?

A

“Barriers to infection”, they are general barriers to all pathogens and are a part of the “non-specific immune system”. This includes:
. Skin - it prevents pathogens from entering the body and secretes a sebum which is slightly acidic
. Ears - produce wax which traps pathogens before they reach the eardrum
. Eyes - produce an enzyme called lysozymes which hydrolyse pathogens
. Nose, lungs and genitals - mucous membrane

6
Q

What are the two parts of the immune system?

A

. Non-specific immune system

. Specific immune system

7
Q

What are the differences between the two types of immune response?

A

. Non-specific
- Barriers and phagocytosis
- Respond to any type of pathogen
. Specific
- Less rapid but longer lasting
- Involve lymphocytes (white blood cells)
- Cell mediated response uses T lymphocytes and kills virus infected body cells
- Humoral response uses B lymphocytes which produce memory cells, plasma cells and antibodies to neutralise pathogens and mark them for destruction

8
Q

Define lymphocyte

A

White blood cell that helps a specific immune respons

9
Q

Define phagocyte

A

White blood cell that collect at the site of an infection and begin to breakdown pathogens

10
Q

Define lysozymes

A

Found in white blood cells and eyes, they are digestive enzymes that hydrolyse pathogens

11
Q

Define phagosome

A

Vesicle formed around a particle engulfed by a phagocyte

12
Q

Define antigen presenting cell

A

Cells that mediate the cellular immune response by processing and presenting antigens

13
Q

How does the body detect self and non-self?

A

Each cell has specific glycoproteins and molecules that have specific tertiary structures/antigens. This is what the cells in the immune system to recognise cells as self and non-self. Although this is advantageous for infection there are implications for people who have organ transplants

14
Q

What happens when a correct lymphocyte binds to it’s complimentary antigen?

A

It clones so it can destroy the pathogen

15
Q

How do lymphocytes learn what is self and non-self?

A

During foetal development lymphocytes are constantly bumping into other body cells, Some lymphocytes will be complimentary to some body cells, this would cause an autoimmune disease, so are destroyed. The remaining lymphocytes have receptors that might be able to bind to foreign pathogens

16
Q

Define apoptosis

A

Programmed cell death

17
Q

What is the first step of phagocytosis?

A

The pathogen releases chemoattractants that cause phagocytes to move into the area

18
Q

What is the second step of phagocytosis?

A

Phagocyte has many different type of receptors on its cell surface membrane. One type binds to the antigen on the pathogen

19
Q

What is the third step of phagocytosis?

A

Pathogen is engulfed by the phagocyte and is placed in a vesicle called a phagosome

20
Q

What is the fourth step of phagocytosis?

A

Lysosomes fuse with the vesicle forming a phagolysosome, releasing hydrolytic enzymes

21
Q

What is the fifth step of phagocytosis?

A

Lysosome enzymes hydrolyse the pathogen

22
Q

What is the sixth and seventh step of phagocytosis?

A

The phagocyte becomes an antigen presenting cell by moving the antigens to the cell surface membrane

23
Q

Define receptor

A

A protein which binds to a specific molecule

24
Q

B lymphocytes

A

Produced and matured in the bone marrow. B cells are involved in humoral immunity. The 3 types are: naive, memory and plasma

25
Q

T lymphocytes

A

Mature in the thymus gland. These are involved in cell mediated immunity, or immunity involving body cells. The 3 types are: helper, memory and cytotoxic

26
Q

What are the 4 steps in cell mediated immunity?

A
  1. Phagocyte presents antigens on its cell surface membrane and is now an antigen presenting cell
  2. A T helper cell with a complimentary receptor binds to the antigen (clonal selection)
  3. Binding stimulates the T helper cell to divide by mitosis (clonal expansion)
  4. The activated T helper cell clones to:
    - Form memory cells to allow a fast response next time
    - Stimulate phagocytes to engulf pathogens
    - Stimulate B cells to divide
    - Activates cytotoxic T cells
27
Q

Define plasma cell

A

A fully differentiated B lymphocyte

28
Q

How do cytotoxic T cells kill infected/cancerous cells?

A

They can produce a protein called perforin which puts holes in the cell-surface membrane and makes it permeable to all substances and the cell dies. Some can also produce hydrogen peroxide which they can move into the targeted cell

29
Q

What is humoral immunity?

A

It involves antibodies which are soluble in blood plasma and tissue fluid. When infected by a pathogen there will be a B cell that is complimentary to the antigen and they will bond together. The antigen is engulfed by the B cell and gets processed. A T helper cell binds to the processed antigen and stimulates the cells to divide by mitosis to form clones

30
Q

Define monoclonal antobosies

A

Identical antibodies from a clone

31
Q

Define clonal selection

A

A T helper cell with a complimentary receptor binds to an antigen

32
Q

Define endocytosis

A

The taking in of matter by a living cell

33
Q

Memory B cells

A

Circulate in the tissue fluid and blood plasma. When they bond to an antigen they have already encountered, they divide rapidly into plasma cells and more memory cells. These cells are involved in long lasting immunity

34
Q

Plasma cells

A

These cells secrete a large amount of antibodies into the blood plasma. These antibodies lead to the destruction of a pathogen

35
Q

What is the first step in immunity?

A

The surface antigens of the pathogen are engulfed by a a naive B cell

36
Q

What is the second step in immunity?

A

The B cell processes the antigen and presents it on its cell-surface membrane

37
Q

What is the third step in immunity?

A

An activated T helper cell binds to the processed antigen on the B cell, and releases cytokines (this is clonal selection)

38
Q

What is the fourth step in immunity?

A

This causes the B cell to divide by mitosis and to produce and secrete a specific antibody

39
Q

What is the fifth step in immunity?

A

The antibody binds to the antigen on the pathogen, and destroys the pathogen

40
Q

What is the sixth step in immunity?

A

Some B cells become memory cells, these recognise and antigen on the 2nd infection divide rapidly to produce more plasma cells so more antibodies are produced and secreted in a shorter time

41
Q

How do antibodies destroy pathogens?

A

. Agglutination - sticking pathogens together
. Neutralisation - blocking the antigens viruses use to infect cells
. Opsonisation - marking the pathogen for phagocytosis

42
Q

How are monoclonal antibodies used as cancer treatment?

A

Monoclonal antibodies are not toxic and specific to certain cells there are few side effects compared with other treatments like chemotherapy. The monoclonal antibody can be attached to a drug or radioactive molecule to be delivered to the cancerous cells to be killed when the antibody binds to the cell

43
Q

How are monoclonal antibodies used in diagnosis?

A

Monoclonal antibodies are used in the diagnosis of 100’s of diseases likw chlamidia and prostate cancer by using an antibody that binds to the antigens that the disease causes to be moved in the blood

44
Q

How are monoclonal antibodies used in pregnancy tests?

A

. The placenta produces the hormone hCG (human chorionic gonadotropin) which is excreted in the woman’s urine
. The hCG binds to the first anti-hCG antibody (which contains a colour changing enzyme) and travels up the strip
. In the test region there is immobilised anti-hGC which binds to the alternatives sites on hCG trapping the antibody-antigen complex. The enzyme causes a colour change showing a positive test
. At the top of the test in the control region unbound antibodies bind to a third antibody causing a colour change showing the test has worked

45
Q

How are monoclonal antibodies used in ELISA test?

A

Antigens get placed in a beaker to be bound to the bottom, the beaker is rinsed to remove any unbound antigens that could give a false result. A solution is then added, any antibodies for the disease we are testing for will bind to the antigens and then washed to make sure any unbound antibodies get removed. A second antibody with a marker is placed in the beaker, and then the beaker is washed again, a positive test will result in a colour change in the marker when the correct substance is added

46
Q

Define hybridoma cell

A

A lymphocyte fused with a tumour cell

47
Q

Define ELISA

A

Designed for detecting and quantifying

48
Q

What is the first step in the production of monoclonal antibodies?

A

Tumour cells are injected into a mouse to stimulate production of B cells, which produce different types of antitumour antibodies

49
Q

What is the second step in the production of monoclonal antibodies?

A

Immortalised myeloma cells are collected

50
Q

What is the third step in the production of monoclonal antibodies?

A

The B cells are fused with the myeloma cells to produce immortalised, antibody-producing hybrid cells (hybridoma)

51
Q

What is the fourth step in the production of monoclonal antibodies?

A

The hybrid cell that produces the needed antibody is selected and cloned to produce unlimited quantities

52
Q

Define passive immunity

A

Antibodies from another source are introduced (breast milk, anti-venom etc…) to acquire immunity. This is fast acting but only short term as no memory cells are made

53
Q

Define active immunity

A

The person stimulates the production of antibodies and memory cells. This takes time to start acting but is long lasting as memory cells are made

54
Q

What are the two types of active immunity?

A

. Natural acting immunity - person contracts an infectious disease
. Artificial acting immunity - a person is vaccinated or immunised

55
Q

What would a good vaccination programme look like?

A

. Must be given before the person contracts a disease
. The vaccine must be cheap enough to produce in large quantities so a large proportion of the population can be immunised
. There are a few, if any side effects
. Producing, storing, transporting and sorting the vaccine must be easy
. Administering the vaccine must be easy and people must be trained
. A large amount of the population must be vaccinated to provide herd immunity, to protect those who are too young, sick or old to be vaccinated

56
Q

Define herd immunity

A

When a large number of the population are vaccinated, . It prevents the spread of disease in a population. Through herd immunity we can protect those that cannot be immunised

57
Q

Why don’t vaccinations always work?

A

. They don’t cause immunity in some because of defective immune systems
. Some people could catch the infection before their immunity levels are high enough to protect them
. Some pathogens change their antigens suddenly due to mutations meaning the old vaccines don’t work, because the memory cells do not recognise the new antigens
. Many different varieties of pathogen so they can’t make a vaccine
. Some pathogens hide inside cells

58
Q

Name 5 ethical issues associated with vaccines

A
  1. Developing and testing involves use of animals
  2. Human testing
  3. Side effects that could cause long term harm
  4. Should vaccination be compulsory if society benefits?
  5. Loss of genetic variability
59
Q

HIV

A

Human Immunodeficiency Virus

60
Q

AIDS

A

Acquired ImmunoDeficiency Syndrome

61
Q

What is the first step in HIV replication?

A

HIV enters the blood stream

62
Q

What is the second step in HIV replication?

A

Proteins (GP120 and GP41) on the outside of the lipid envelope of HIV bind to CD4 which is found on T helper cells

63
Q

What is the third step in HIV replication?

A

The lipid envelope and the cell surface membrane of the T helper cell fuse together, and the capsid is released into the T helper cell

64
Q

What is the fourth step in HIV replication?

A

The RNA and reverse transcriptase are released into the cytoplasm of the cell, where reverse transcriptase makes ssDNA from mRNA

65
Q

What is the fifth step in HIV replication?

A

Complementary base pairing occurs between free DNA nucleotides and ss cDNA

66
Q

What is the sixth step in HIV replication?

A

DNA polymerase joins the DNA nucleotides together and make dsDNA

67
Q

What is the seventh step in HIV replication?

A

Newly made viral DNA is inserted into the T helper cells genome

68
Q

What is the eighth step in HIV replication?

A

The HIV DNA in the nucleus is used to make mRNA. This mRNA holds the instructions for making new virus capsids, copies of the mRNA genome, and the enzymes to make new HIV virions

69
Q

What is the ninth step in HIV replication?

A

The mRNA moves out of the nucleus to a ribosome to make the viral proteins

70
Q

What is the tenth step in HIV replication?

A

The virus is assembled and buds off the T helper cell, surrounded in the membrane of the T helper cell, this is the lipid envelope

71
Q

How does HIV cause AIDS?

A

HIV kills the T helper cells in the blood, when the number of T helper cells drops to 200 per mm3 of blood the person has AIDS

72
Q

Define reverse transcriptase

A

Enzyme used to generate complimentary DNA from an RNA template

73
Q

Define capsid

A

Protein shell of a virus

74
Q

Define retrovirus

A

Type of RNA virus that inserts a copy of its genome into the DNA of a host cell that it invades

75
Q

How do bacteria become resistant to bacteria?

A

. Bacteria replicates quickly increasing the chance of mutations
. Bacteria that is resistant to the bacteria survives and passes the advantageous allele onto its offspring (vertical gene transfer)
. Bacteria can transfer genes horizontally (within the same generation) by sharing plasmids