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Biology A Level > Immunity > Flashcards

Immunity Flashcards

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1
Q

What is an infection?

A

An interaction between the pathogen + body’s various defence mechanisms?

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2
Q

What is immunity?

A

After an individual has survived a pathogen infection before, the individual is better prepared for a second infection from the same pathogen and can kill it before it does any harm.
Main reason some people = unaffected by certain pathogens.

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3
Q

What does immunity depend on?

A

Overall health of person.
Fit healthy adult - rarely die of an infection.
Ill health = more vulnerable usually.

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4
Q

What are the two types of defences a body has from disease?

A

Specific responses.

Non-specific responses.

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5
Q

What are non-specific responses?

A

Immediate response + same for all pathogens. Take 2 forms:
Physical barrier, e.g. Skin.
Phagocytosis.

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6
Q

What are specific responses?

A

Slower response + specific to each pathogen. Take 2 forms:

Cell-mediated response - T lymphocytes. Humoral response - B lymphocytes.

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7
Q

What are antigens?

A

Any part of an organism/substance recognised as non-self (foreign) by immune system + stimulates an immune response.
Usually - Proteins on cell-surface membrane/ cell wall of every invading cell.
Presence of an antigen triggers production of an antibody as part of body’s defence system.

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8
Q

How do cells distinguish between one another?

A

Proteins on surface have enormous variety + very specific tertiary shape, .: variety of 3D shape allows cells to distinguish between one another.

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9
Q

What do antigens on cell surface allow immune system to do?

A 
Identify:
Pathogens,
Donor cells/non-self material. 
Toxins. 
Abnormal body cells, e.g. Cancer cells.
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10
Q

What affect does the immune system have on donor transplants?

A

Immune system recognises it as non-self material + tries to destroy transplant.

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11
Q

How are the effects of immune system on donor transplants minimised?

A

Donor tissues for transplants = closely matched to recipient - best = relatives.
Immunosuppressant drugs monitored to reduce immune response level that still occurs.

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12
Q

What is clonal selection?

A

When one type of lymphocyte which has complementary proteins to those of pathogen infecting body is stimulated to divide - build up its numbers.

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13
Q

What does clonal selection explain?

A

Time lag between pathogen exposure and body’s defences controlling it.

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14
Q

What is the body’s first line of defence against infection?

A

Physical/chemical barriers, e.g. Skin.

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15
Q

What is the body’s second line of defence?

A

If first line of defence fails, second line of defence = lymphocytes + more specifically phagocytosis.

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16
Q

What is phagocytosis?

A

When large particles, e.g. Some types of bacteria, are engulfed by cells in vesicles formed from cell-surface membrane.

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17
Q

What are the steps of phagocytosis?

A

Phagocyte = attracted to pathogen by chemical products of pathogen so moves towards pathogen along conc. gradient.

  1. Phagocytes have several receptors in cell-surface membrane - recognise + attach to chemicals on pathogen.
  2. Phagocyte engulfs pathogen - forms a vesicle = known as a phagosome. Lysosomes in phagocyte move towards to vesicle + fuse with it.
  3. Lysosomes release lysozymes + destroy bacteria by hydrolysing their cell walls.
  4. Soluble products from bacteria cell walls = absorbed into cytoplasm of phagocyte.
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18
Q

How do cytotoxic T cells kill infected cells?

A

Produce a protein called perforin - makes holes in cell-surface membrane -> .: freely permeable to all substances + .: cell dies.

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19
Q

What are T cells most effective against and why?

A

Viruses.

They replicate inside cells - sacrifice of body cells prevents viruses multiplying + infecting more cells.

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20
Q

What are the stages of humoral immunity?

A
  1. Surface antigens of invading pathogens = taken up by B cells.
  2. B cells process + present antigens on their surface.
  3. Helper T cells attach to processed antigens on B cell, .: Activates B cells.
  4. B cells = activated to divide by mitosis = clone of plasma cells.
  5. Cloned plasma cells produce/secrete antibody which = complementary to antigen on pathogen’s surface.
  6. Antibody attaches to antigen on pathogen + destroys it.
  7. Some B cells -> memory cells - respond to future infections by -> plasma cells - produce antibodies = secondary immune response.
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21
Q

How do memory cells work?

A

Once memory cells meet the same antigen which caused original infection, they divide rapidly into plasma cells + memory cells.
Plasma cells produce antibodies - destroy pathogen.
New memory cells circulate blood/tissue fluid ready for future infection.
Long-term immunity against original infection.
Ensures new infection = destroyed before it can cause harm. Individuals = often unaware that they’ve been infected.

22
Q

How are monoclonal antibodies produced?

A

Antibody attaches to complementary antigen. Antigen enters B cell by endocytosis + is represented on cell surface.
T cells bind to antigen stimulating the B cells to divide by mitosis producing clones of the B cells = clonal selection.
These B cells all carry the same antibody so therefore many antibodies which are all clones of one another are produced = monoclonal antibodies.

23
Q

What do plasma cells do in humoral immunity?

A

Release antibodies to blood plasma usually.
Survive for few days lonely.
Make many antibodies to destroy antigens.
Immediate defence of body against disease = primary immune response.

24
Q

What do memory cells do in humoral immunity?

A

Secondary immune response.
Live longer than plasma cells.
Don’t directly form antibodies (circulate blood/tissue fluid). When meet antigen, they divide by mitosis into plasma cells (produce antibodies) + memory cells (circulate- ready for future infection).
Long-term immunity against infection.
More antibodies released than primary response.

25
Q

What are antibodies?

A

Proteins with specific binding sites synthesised by B cells.

26
Q

What are monoclonal antibodies?

A

When you can produce antibodies outside of body + single antibody be isolated + cloned.
Great medical value and has many uses in science + medicine.

27
Q

What are some uses of monoclonal antibodies?

A

Targeted medication - direct + indirect monoclonal antibody therapy.
Medical diagnosis.
Pregnancy testing.

28
Q

What is the process of direct monoclonal antibody therapy for cancer?

A
  1. Monoclonal antibodies produced = specific to antigens on cancer cells.
  2. These antibodies = given to patient + attach to receptors on their cancer cells.
  3. They attach to surface of cancer cells + block chemical signals which stimulate uncontrolled growth.
29
Q

What is the advantage of direct monoclonal antibody therapy?

A

Not toxic + highly specific, so lead to fewer side effects than other forms of therapy.

30
Q

What is the process of indirect monoclonal antibody therapy for cancer?

A

Attach radioactive/cytotoxic drug to monoclonal antibody.
When antibody attaches to cancer cells it kills them.
Called ‘magic bullets’.
Used in smaller doses as they target specific areas.

31
Q

What is the advantage of indirect monoclonal antibody therapy?

A

Smaller doses = cheaper + less side effects.

32
Q

What are the ethics involved with use of monoclonal antibodies?

A

Production of them involves using mice to produce antibodies + tumour cells. To get tumour cells mice are deliberately induced with cancer. Some people may have reservations about using animals in this way.
Have been some deaths associated with use in treatment of multiple sclerosis. Important patients have full knowledge of benefits + risks of drugs before giving permission for them to be used (=informed consent).
Testing for safety of new drugs has certain dangers - raises issues about conduct of drug trials.

33
Q

What is passive immunity?

A

Receive the antibodies from external source. No direct contact with pathogen/antigen needed.
Antibodies not replaced/broken down. No memory cells formed. No lasting immunity.
E.g. Antibodies passed from mother’s placenta to fetus/ from mother’s breast milk to enfant.

34
Q

What is active immunity?

A

Stimulating production of antibodies by individuals’ own immune system.
Direct contact with antigen/pathogen = necessary.

35
Q

What are the 2 types of active immunity and explain them?

A

Natural active immunity - individuals become infected with disease under normal circumstances.
Artificial active immunity - basis of vaccination - induce immune response without them suffering symptoms of disease.

36
Q

What is a vaccination?

A

Introduction of appropriate disease antigens to body by injection/mouth.
Intention = stimulate immune response from disease.

37
Q

What is a vaccine?

A

Material introduced in vaccination - contains 1 or more types of antigen from pathogen.

38
Q

Describe a vaccination.

A
  1. Dead/weakened (attenuated) pathogen antigens introduced to individual to induce an immune response.
  2. Memory cells produced.
  3. Future infection by same pathogen, produces a greater, more immediate response.
39
Q

What features does the success of a successful vaccination programme depend on?

A
  1. Vaccine being economically available in sufficient quantities to immunise most of vulnerable populations.
  2. Few if any side effects. Unpleasant side effects may discourage individuals to have vaccination.
  3. Means of producing, storing + transporting vaccine.
  4. Means of administering vaccine properly at appropriate time - staff with appropriate skills available in diff. centres in population.
  5. Vaccine majority of vulnerable population - produce herd immunity.
40
Q

What is herd immunity?

A

Resistance to spread of contagious disease in a population = sufficiently high proportion of individuals = immune to disease through vaccination.
Best done all at one time - at one time few individuals have disease .: transmission of pathogen = interrupted.

41
Q

Why aren’t vaccines always effective?

A
  1. Fails to reduce immunity in certain individuals, e.g. Defective immune system.
  2. May develop disease in vaccination - harbour vaccines + reinfect others.
  3. Pathogens mutate frequently - antigens change suddenly NOT gradually - vaccines = suddenly ineffective - immune system doesn’t recognise it/ produce antibodies to destroy it due to antigenic variability.
  4. Too many varieties of pathogens to create a vaccine for them all.
  5. Some pathogens ‘hide’ in cells/places out of reach from immune system.
  6. Individuals may have objections to vaccination for religious, ethical or medical reasons.
42
Q

What are the ethics involved with vaccinations?

A
  1. Often uses animals.
  2. Has many side-effects.
  3. Individuals risk lots in trials for vaccinations.
  4. Targeting untested vaccines in areas where targeted disease is common.
  5. All population should be vaccinated to be effective. Not everybody wants this due to religious belief, medical circumstances or personal belief.
  6. Expensive - less money for treatment of other diseases.
  7. Individuals risk their health for a bit when injected with a vaccine.
43
Q

Describe the structure of the Human Immunodeficiency Virus (HIV).

A

Has lipid balayer on outside layer with attachment proteins.
Inside envelope = protein layer called capsid. In this are 2 single strands of RNA + enzymes - one of which = reverse transcriptase (RNA->cDNA->DNA).

44
Q

Why is HIV classed as a retrovirus?

A

It has reverse transcriptase enzyme.

Can .: convert RNA back into DNA.

45
Q

How does HIV replicate?

A
  1. After infection, HIV enters bloodstream + circulates body.
  2. HIV protein readily binds to CD4 protein - by a helper T cell.
  3. Protein capsid fuses with cell-surface membrane. RNA + HIV’s enzymes enter helper T cell.
  4. HIV’s reverse transcriptase convert’s virus’s RNA -> DNA.
  5. DNA moves to T cell’s nucleus = inserted into cell’s nucleus.
  6. HIV DNA in nucleus creates mRNA using cells enzymes = instructions make viral proteins + RNA for new HIV molecules.
  7. mRNA leaves nucleus via nucleus pores + uses cells protein synthesis mechanisms to make HIV particles.
  8. HIV particles break away from helper T cells with bit of cell-surface membrane which forms their lipid envelope.
46
Q

What is it called when someone is infected with HIV?

A

HIV positive.

HIV replication goes dormant after a while but recommences leading to AIDS, years later.

47
Q

How does HIV cause AIDS symptoms?

A

Attacks helper T cells - interferes with normal functioning of helper T cells. Without sufficient no. of T cells, immune system can’t stimulate B cells to produce antibodies/cytotoxic T cells - kill cells infected by pathogens. Memory cells = infected + destroyed.
.: Body = unable to produce adequate immune response + become susceptible to other infections + cancer. .: Individual doesn’t die from HIV itself but because they are susceptible to other diseases from weakened immune system so die from other diseases.

48
Q

What does the ELISA test test for?

A

To detect presence of a protein and quantity of protein.
For drug and allergen tests.
Detect HIV + pathogens of diseases, e.g. Tuberculosis + hepatitis.
Especially useful to find out antigen quantity.

49
Q

What is the process of the ELISA test?

A
  1. Apply sample to surface which all enzymes will attach.
  2. Wash surface several times - remove unattached antigens.
  3. Add antibody specific to antigen we’re detecting + leave to bind together.
  4. Wash surface to remove excess antibody.
  5. Add second antibody with enzyme attached to it - binds with first antibody.
  6. Add colourless substrate of enzyme. Enzyme acts on substrate + changes it to a coloured product.
  7. Amount of antigen present = relative to intensity of colour developed.
50
Q

Why are antibodies ineffective against viral infections like HIV?

A

One way antibodies work = preventing bacterial cells from making cell walls.
HIV has:
No metabolic mechanisms.
No cell structures.
Protein coat not cell wall - means they can’t prevent them from making cell walls as they don’t have one in the first place.
No sites for antibiotics to target.
Place to hide in host cells.

Biology A Level (13 decks)

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