5. Cell Recognition and the Immune System Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

Describe the process of cell-mediated immunity

A

Main cell= T lymphocyte

  1. Pathogens invade body cells or are taken in by phagocytes.
  2. The phagocyte places antigens from the pathogen onto its cell surface membrane (antigen presenting cell).
  3. Receptors on a specific helper T cell fit exactly into the antigens.
  4. The attachment activates the T cell to divide rapidly by mitosis and form a clone of genetically identical cells.
  5. The cloned T cells:
    - develop into memory cells that engage a rapid response to future infection by the same pathogen.
    - stimulate phagocytosis
    - stimulate B cells to divide and secrete antibodies
    - activate cytotoxic/killer T cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the process of humoral immunity

A

Main cell= B lymphocyte

  1. The antigens of an invading pathogen are taken up by a B cell.
  2. The B cell processes antigens and presents them on its surface (antigen presenting cell).
  3. Helper T cells (activated by cell mediated response) attach to the processed antigens on the B cell, thereby activating the B cell.
  4. The B cell is now activated to divide by mitosis to give a clone of plasma cells.
  5. The cloned plasma cells produce and secrete the specific antibody that fits the antigen on the pathogen’s surface.
  6. The antibody attaches to antigens on the pathogen and destroys them.
  7. Some B cells develop into memory cells. These respond to future infections by the same pathogen by dividing rapidly and developing plasma cells that produce antibodies. This is the secondary immune response.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define the term ‘pathogen’

A

Any microorganism that causes disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define the term ‘immunity’

A

The means by which the body protects itself against infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define the term ‘phagocytosis’

A

Mechanism by which phagocyte cells engulf particles to form a vesicle or vacuole.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Define the term ‘lymphocyte’

A

Types of white blood cell responsible for the immune response. They become activated in the presence of antigens. Two types- B and T.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Define the term ‘cell mediated immunity’

A

Response of T-lymphocytes to antigens presented on a body cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Define the term ‘humoral immunity’

A

Response of B-lymphocytes to antigens in the blood/tissue fluid. Involves antibodies, soluble in body fluids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define the term ‘memory cell’

A

Memory cells can live for many years, up to decades, remaining into the blood, ready to trigger an immune response if encountering the same pathogen again. Can induce long-term immunity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a primary immune response?

A

The production of antibodies and memory cells, when a B lymphocyte undergoes immune response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a secondary immune response?

A

Memory cells can stay circulating in the blood for decades. When they encounter the same antigen at a later date, they divide rapidly and produce plasma cells and more memory cells. The plasma cells produce the complimentary antibodies needed to destroy the specific pathogen, while the new memory cells circulate in readiness for future infection. The secondary response secretes an increased quantity of antibodies at a faster rate, destroying the infection before it causes harm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Define the term ‘passive immunity’

A

Resistance to disease that’s acquired from the introduction of antibodies from another individual, rather than an individual’s own immune system, usually short lived. E.g. across placenta or mothers milk.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Define the term ‘vaccination’

A

The introduction of a vaccine containing an appropriate amount of disease antigens into the body, by injection or mouth, in order to induce artificial immunity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Define ‘self material’

A

The body’s own cells and molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Define ‘non self material’

A

Foreign cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is ‘clonal selection’?

A

T-helper cells bind to processed antigens, stimulating the B-cell to divide by mitosis, to form a clone of identical B cells, all of which produce the antibody specific to the foreign antigen. Accounts for the body’s ability to respond rapidly to a vast number of antigens.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give an example where immune response to non-self material is disadvantageous

A

Humans who have had tissue/organ transplants.
The immune system recognises as non-self, despite coming from the same species, and therefore attacks and tries to destroy the transplant. To minimise the effect of rejection, donors are closely matched to the recipient and immunosuppressant drugs are given.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Define the term ‘heavy chains’

A

Pair of long polypeptide chains that make up quaternary structure of antibodies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Define the term ‘light chains’

A

Pair of short polypeptide chains that make up quaternary structure of antibodies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Define the term ‘variable region’

A

The binding site on antibodies, different for every antibody.
(Rest of antibody= constant region. Bind to receptors on cells such as B-cells)

21
Q

Define the term ‘passive immunity’

A

Resistance to disease that’s acquired from the introduction of antibodies from an outside source, rather than an individual’s own immune system, no direct contact necessary to induce immunity & usually short lived. E.g. across placenta or mothers milk.

22
Q

Define the term ‘natural active immunity’

A

Involves direct contact with pathogen/antigen. Individual is infected with a disease under normal circumstances. The body produces its own antibodies and may continue to do so for many years.

23
Q

Define the term ‘artificial active immunity’

A

Involves direct contact with pathogen/antigen. Forms the basis of vaccination, involving inducing an immune response in an individual, without them suffering from the disease.

24
Q

Define the term ‘herd immunity’

A

When a large proportion of the population has been vaccinated to make it difficult for a pathogen to spread within that population. Where vast majority of the population is immune, its impossible that a susceptible individual will come into contact with an infected person. Therefore, individuals not immune to the disease are protected.

25
Q

Define the term ‘antigenic variability’

A

Pathogens can mutate frequently, so antigens change suddenly.

26
Q

Suggest why lysozymes are found in tears

A

The protective covering of the eye and the tear ducts are entry points for pathogens. The eyes are vulnerable to infection because the coverings are thin to allow light through. Lysozyme breaks down the cell walls of any bacterial pathogens and will destroy them before they cause harm.

27
Q

Where do B Lymphocytes mature?

A

Bone marrow

28
Q

Where do T Lymphocytes mature?

A

Thymus gland

29
Q

How do cytotoxic T cells kill infected cells?

A

Produces a protein called perforin, that makes hole in the cell surface membrane, making the membrane permeable to all substances, causing the cell to die.

30
Q

What are plasma cells?

A

Plasma cells are produced by B-lymphocytes, and secrete up to 2000 antibodies into the blood plasma.

31
Q

State two similarities between T and B lymphocytes

A
  • Both are white blood cells

- Both produced from stem cells

32
Q

State two differences between T and B lymphocytes

A
  • T cells mature in thymus gland, B cells mature in bone marrow.
  • T cells are involved in cell-mediated immunity, B-cells are involved in humoral immunity
33
Q

Explain why the secondary immune response is much more rapid than the primary response.

A

In the primary response, the antigens of the pathogen have to be ingested, processed and presented by B cells. Helper T cells need to link with B cells to activate them so they can clone, developing into plasma cells producing antibodies and memory cells. These processes happen consecutively and therefore take time.
In the secondary response, memory cells are already present, only the processes of cloning and development into plasma cells that produce antibdies. Fewer processes means a quicker response.

34
Q

Contrast the cell-mediated and humoral responses to a pathogen

A

Cell mediated immunity involves T cells, Humoral immunity involves mostly B cells.
Cell mediated immunity doesn’t involve antibodies, Humoral immunity produces antibodies.
Cell-mediated immunity only gives the first stage of immune response, Humoral immunity gives the second stage of immune response after cell meditated stage.

35
Q

Plant cells produce up to 2000 protein antibodies each second. Suggest 3 organelles you expect to find in large quantities and why.

A

Rough endoplasmic reticulum- to make and transport antibody proteins.
Golgi apparatus- to sort, process and compile the proteins.
Mitochondria- to release energy needed for such massive antibody production.

36
Q

How do antibodies lead to antigen destruction.

A
  • Cause agglutination of pathogenic cells. So clumps of pathogenic cells are formed, making it easier for phagocytes to find them within the body.
  • They then serve as markers that stimulate phagocytes to engulf cells to which they’re attached.
37
Q

Describe how monoclonal antibodies treat cancer by direct monoclonal antibody therapy.

A
  • Monoclonal antibodies are produced that are specific to antigens on cancer cells.
  • These antibodies are given to a patient and attach themselves to receptors on their cancer cells.
  • They attach to the surface of their cancer cells and block the chemical signals that stimulate their growth.
38
Q

Describe how monoclonal antibodies are used in pregnancy testing.

A

The placenta produces a pregnancy hormone hCG, present in the mothers urine.
Monoclonal antibodies are linked to coloured particles on the pregnancy test strip.
If hCG is present in the urine it binds to the antibodies.
The hCG antibody-colour complex moves along the strip until trapped by a second antibody, creating a coloured line. If hCG not present the coloured particles will not stick to the strip.

39
Q

State some ethical issues with monoclonal antibodies

A
  • Involves use of mice, used to produce antibodies and tumour cells. Involves inducing cancer on the mice.
  • Risks and benefits- successful in treating cancer and diabetes, but deaths associated with treatment of multiple sclerosis.
  • Safety testing can be dangerous. March 2006 trials 6 healthy volunteers suffered organ failure within minutes of taking drug, raising issues about conduct of drug trials.
40
Q

How are monoclonal antibodies produced?

A
  • Mouse exposed to non-self material against which an antibody is required.
  • B cells produce a mixture of antibodies, extracted from the spleen of the mouse.
  • B cells mixed with tumour cells so they divide readily outside the body
  • Detergent added to break down cell membranes and fuse both cells together, forming hybridoma cell.
  • Hybridoma cell separated and each cell cultured to form a clone, each tested to see if producing the antibody required
  • Any clone producing required antibody grown on a large scale and ‘monoclonal’ antibodies extracted.
41
Q

Suggest why antibodies made of proteins are most likely to be effective against a wide range of diseases

A

There must be a massive variety of antibodies as each responds to a different antigen, of which there are millions. Only proteins have the diversity of molecular structure to produce millions of different types of antibody.

42
Q

Give features of a successful vaccination programme

A
  • Suitable vaccine economically available in sufficient quantities to immunise most of the population.
  • Few side effects if any, as may discourage people.
  • Means of producing, storing and transporting vaccine. Involves technological equipment, hygienic conditions and refrigerated transport.
  • Means of administrating the vaccine- trained staff
  • Must be possible to vaccine majority of vulnerable population to produce herd immunity.
43
Q

Why might a vaccine be unsuccessful in eliminating a disease

A
  • Fails to induce immunity for certain individuals, e.g. people with defective immune systems.
  • Individuals may develop the disease immediately after vaccination before their immunity levels are high enough to protect, and can spread it to others.
  • Antigenic variability causes vaccines to suddenly be ineffective as the new antigens on the pathogen are no longer recognised, and the immune system doesn’t produce antibodies to destroy the pathogen.
  • Many varieties of a pathogen so impossible to develop a vaccine effective against them all.
  • Pathogens can ‘hide’ from the immune system.
  • Individuals may object due to ethical, religious or medical reasons.
44
Q

What are the ethical issues of vaccines?

A
  • Development and production often involves animals.
  • May have side effects causing long term harm
  • Conduct of trials- who tested? how carried out? should individuals take risk in interest for public health?
  • Acceptable to trial a vaccine only in a country where the disease is common?
  • To be fully effective most of the population should be vaccinated. should it be compulsory?
  • Should vaccination programmes continue when disease is almost eradicated, despite meaning less money for treatment of other disease?
45
Q

How does HIV replicate?

A
  • Following infection, HIV enters the bloodstream and circulates around the body.
  • A protein on HIV readily bonds to the protein CD4-most frequently attaching to T helper cells.
  • Protein capsid fuses with the cell-membrane. RNA and enzymes of HIV enter T helper cell.
  • HIV reverse transcriptase converts virus’ RNA to DNA
  • The DNA moves into the helper T cell’s nucleus, and inserts into the cell’s DNA.
  • The HIV DNA in the nucleus creates mRNA, containing the instructions for making new viral proteins and the RNA enter the new HIV.
  • The mRNA passes out of the nucleus through nuclear pore and uses the cell’s protein synthesis mechanisms to make HIV particles.
  • The HIV particles break away from the T helper cell with a piece of its cell-surface membrane forming their lipid envelope.
46
Q

Why are antibiotics ineffective against viral diseases, like HIV/AIDS?

A

Viruses rely on host cells to conduct metabolic activities, so lack their own metabolic pathways and cell structures. Therefore antibiotics are ineffective as there are no metabolic mechanisms or cell structures for them to disrupt.
Viruses have a protein coat rather than a murein cell wall, so no sites for antibiotics to work.
When viruses are within an organisms own cells, antibiotics can’t reach them.

47
Q

Why is HIV a retrovirus?

A

It possesses RNA and the enzyme reverse transcriptase which can make DNA from RNA- a reaction reverse of that carried out by transcriptase.

48
Q

How does HIV cause symptoms of AIDS?

A

HIV specifically attacks T-helper cells. An uninfected person has 800-1200 T-helper cells in each mm3 of blood, whereas someone suffering with AIDS can have as low as 200. With insufficient helper T cells the body is unable to stimulate B cells to trigger antibody response, create cytotoxic T cells or memory cells. Therefore the individual has an extremely low immunity, becoming susceptible to infection.

49
Q

How is the ELISA test carried out to detect HIV and its quantity?

A

Apply the sample to a slide, to which the antigens in the sample will attach to the surface.
Wash the slide several times to remove any unattached antigens.
Add the antibody specific to the HIV antigen, and leave the sample so the two can bind to form an antigen-antibody complex.
Wash the slide again to remove excess antibody.
Add a second antibody, attached to an enzyme, to bind with the first antibody.
Add the colourless substrate of the enzyme. The enzyme acts on the substrate, changing it into a coloured enzyme-substrate complex.
The amount of HIV antigen present is relative to the amount of colour that develops.