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Biology: 3.2 Cells > 3.2.4 Cell Recognition & The Immune System > Flashcards

3.2.4 Cell Recognition & The Immune System Flashcards

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1
Q

(Cell Recognition & Immunity) What are the key features of your innate immune system?

A

Non-specific (no B / T cells)
Immediate
Same for all pathogens

  • Physical and chemical barriers e.g. hydrochloric acid in stomach, skin, ciliated epithelium in the airways
  • Phagocytes
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2
Q

(Cell Recognition & Immunity) Detail the process of phagocytosis. (9)

A

Phagocyte e.g. macrophage
Pathogen e.g. bacteria release toxins
Phagocyte engages chemotaxis using protein receptors in its cell surface membrane
Endocytosis on binding with pathogen
Phagosome (vesicle) containing pathogen
Lysosomes contain hydrolytic lysozymes (e.g. proteases)
Fusion forming phagolysosome / phagocytic vacuole
Digestion by hydrolysis
Release of contents by exocytosis

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3
Q

(Cell Recognition & Immunity) What is an antigen?

A
  • Molecules, which when recognised as non-self (foreign) by the immune system, can stimulate an ‘immune response’ thus producing antibodies
  • Often proteins on the surface of cells or viruses
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4
Q

(Cell Recognition & Immunity) Proteins have a specific ‘tertiary structure’. What does this cause them to be?

A

Antigens.

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5
Q

(Cell Recognition & Immunity) What do cell surface molecules enable the immune system to identify? (5)

A
  • Pathogens (disease causing organisms) e.g. viruses, bacteria, fungi
  • Cells from other organisms of the same species e.g. organ transplant, blood transfusion
  • Pathogens contained in vacuoles / vesicle / phagosomes within phagocytes
  • Toxins released from bacteria
  • Abnormal / cancerous cells
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6
Q

(Cell Recognition & Immunity) What is an antibody/antibody-antigen complex?

A

Proteins produce by B lymphocytes / plasma cells…

2 longer, heavy chains bonded to 2 lighter chains via disulphide bonds

Constant region

Highly variable region acting as ‘antigen binding site’

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7
Q

(Cell Recognition & Immunity) Regarding an antibody/antibody-antigen complex what does each B cell produce?

A

A different antibody.

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8
Q

(Cell Recognition & Immunity) Regarding an antibody/antibody-antigen complex what can each antibody bind to?

A

One specific antigen shape.

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9
Q

(Cell Recognition & Immunity) Regarding the specific immune response, detail the cell mediated response.

A

Phagocytes present antigen to T cells
Matching T cell receptors on T helper and T cytotoxic cells
T helper cells release cytokines
T cytotoxic cells undergo clonal expansion / mitosis
T cytotoxic cells bind to antigen and destroy pathogen / infected cell / cancerous cell by releasing perforin

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10
Q

(Cell Recognition & Immunity) Regarding the specific immune response, detail the humoral / antibody mediated response.

A

Phagocytes present to B lymphocytes
B cell have antibody receptors in their cell surface membrane
Specific B cell binds to specific antigen
B cell engulfs antigen by endocytosis, hydrolysed and presented on the cell surface membrane

T helper cells bind to the antigen (peptide) on the specific B cell, releasing cytokines
Specific B cell undergoes clonal expansion / mitosis to form many plasma cells
Plasma cells produce and release matching antibodies
Antibodies can form antibody-antigen complexes - agglutination, opsonization, neutralisation, inactivation

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11
Q

(Cell Recognition & Immunity) Describe active immunity. (5)

A
  • Exposure to antigen either through infection by pathogen or vaccination
  • Stimulates an immune response
  • Antibodies are produced
  • Memory B / T cells produced / long term
  • Memory cells will recognise antigen / pathogen if exposed in future leading to a rapid immune response

e.g. measles virus

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12
Q

(Cell Recognition & Immunity) Describe passive immunity. (5)

A
  • Antibodies only
  • No exposure to antigen
  • No immune response
  • No memory B / T cells
  • Immediate protection / short term

e.g. tetanus toxin

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13
Q

(Cell Recognition & Immunity) Explain the concept of herd immunity.

A

The higher the proportion / percentage a population is vaccinated against a pathogen the lower the probability an infected person will come into contact with an unvaccinated person.

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14
Q

(Cell Recognition & Immunity) Describe suitable vaccines. (4)

A
  • Economically viable
  • Enough cover population in order to obtain herd immunity where possible
  • Produce, store and transport efficiently and without damage
  • Organised administration with trained staff
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15
Q

(Cell Recognition & Immunity) Describe antigenic variability. (4)

A
  • Pathogens mutate
  • Variability alters the antigen shapes on the surface of pathogens e.g. flu
  • Antigenic ‘drift’ gradual alteration (poor immune recognition)
  • Antigenic ‘shift’ significant alteration in shape (no immunity, no recognition)
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16
Q

(Cell Recognition & Immunity) Describe the primary immune response.

A

Primary response is an initial exposure to an unknown antigen resulting in an immune response

Primary response will be slower but produces memory B / T cells (active immunity acquired).

17
Q

(Cell Recognition & Immunity) Describe the secondary immune response.

A

Secondary immune response - memory B / T cells recognise the antigen and respond…
- More rapidly
- More intense / high concentration of antibodies released
- Prolonged

18
Q

(Cell Recognition & Immunity) Why are antibiotics ineffective against viruses?

A

Viruses are acellular (non-living).

Viruses do not have any metabolism.

Antibiotics target bacteria using specific modes of action e.g. affecting murein cell wall production or inhibiting protein synthesis.

19
Q

(Cell Recognition & Immunity) How does the HIV virus replicate? (9)

A

Viral gp120 glycoprotein attachment proteins bind to CD4 receptors on T helper cells.

On entering the host cell reverse transcriptase synthesises cDNA copy of the viruses RNA genome.

Double stranded copy is then produced which integrates into the T helper cell’s chromosomal DNA.

This is proviral DNA.

Proviral DNA acts as a template for the transcription of viral RNA copies.

Translation of viral genes to produce viral proteins e.g. capsid, reverse transcriptase, gp120.

HIV viruses are assembled.

HIV viruses exit the cell by “budding”, removing some of the cell membrane.

This destroys the T helper cell.

20
Q

(Cell Recognition & Immunity) Explain how HIV causes the symptoms of AIDS. (8)

A

Destruction of T helper cells results in an inability to fight infection.

Fewer T helper cells can bind with specific B cells.

Cytokines are not released.

No clonal expansion of B cells.

No plasma cells, so no antibody production against antigen.

No clonal expansion of T cytotoxic cells.

No targeting of antigen in body cells e.g. viral infection, cancerous cells etc.

Opportunistic pathogens can cause disease i.e. AIDS (acquired immunodeficiency syndrome).

21
Q

(Cell Recognition & Immunity) Describe the use of monoclonal antibodies in targeting medication to specific cells.

A

Monoclonal antibodies can bind to one very specific antigen.

They are produced in vitro using hybridoma cells (specific B cells fused with mice cancer cells).

22
Q

(Cell Recognition & Immunity) Describe how monoclonal antibodies are used in therapeutic medicine.

A

Breast cancer cells have specific protein antigen on the cell surface.
Monoclonal antibodies can target these.
Radioactive or cytotoxic drugs can be attached to the monoclonal antibodies thus killing the cancer cells.
Very specific / targeted with limited side effects.

23
Q

(Cell Recognition & Immunity) Describe how monoclonal antibodies are used in medical diagnosis.

A

Pregnancy test, HIV test, prostate cancer diagnosis (PSA protein in blood).

24
Q

(Cell Recognition & Immunity) Describe the use of antibodies in diagnostic ELISA tests.

A
  1. HIV antigen / protein attached to well of test plate
  2. anti-HIV antibodies from infected patient forms antibody-antigen complex with HIV antigen - immobilised

Plate washed to remove any other unbound antibodies…

  1. Enzyme attached anti-human (mouse) antibodies bind to attached anti-HIV antibodies - immobilised

Plate washed to remove unbound antibodies / “free” enzyme complexes…

  1. Immobilised enzyme catalyses reaction producing a coloured substrate (HIV +ve)
25
Q

(Cell Recognition & Immunity) What are the ethical issues associated with monoclonal antibodies? (3)

A

Mice used to produce tumours for antibody production
Informed consent from patients as some deaths linked to use
Clinical trials have significant risks

26
Q

(Cell Recognition & Immunity) What are the ethical issues associated with vaccines? (6)

A

Animal testing
Potential side-effects
Clinical trials
Consent for vaccination vs compulsory need to acquire herd immunity
Expense
Individual health risks vs advantages of controlling a disease for the whole population

27
Q

(Cell Recognition & Immunity) Explain how antibiotic resistance is an example of ‘directional selection’. (8)

A

1) Antibiotics act as a selective pressure
2) Spontaneous, random, gene mutation
3) New protein produced
4) Increased resistance to an antibiotic
5) Resistant bacteria survive and divide by binary fission/reproduce
6) Susceptible bacteria die/outcompeted
7) Frequency of resistant bacteria increases
8) Populations ‘normal distribution’ curve shifts in the direction of the population being more resistant

Biology: 3.2 Cells (4 decks)

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