cells3 Flashcards

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1
Q

What is the primary immune response?

A

= Production of antibodies and memory cells from new B-cells, after antigen enters body for the first time.

Slower, so symptoms of disease shown.

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2
Q

What is the secondary immune response?

A

= Quicker, stronger immune response due to memory cells -> clonal selection happens faster, B-memory cells activated and divide into plasma cells, producing necessary antibody.

Memory T-cells activated and divide into correct T-cells to kill cells presenting the antigen.

Much quicker, so symptoms not usually shown.

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3
Q

Comment on/draw the structure of an antibody.

A

4 polypeptide chains - 2 heavy chains, 2 light chains.

Include antigen-binding sites.

Include constant and variable regions (variable region dependant on antibody).

Include receptor binding site.

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4
Q

Why can we have so many different antibodies?

A

Enormous variety of protein structure -> each binding site consists of a sequence of amino acids, forming a specific tertiary structure and 3D shape that binds directly to a specific antigen, forming an antigen-antibody complex.

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5
Q

Outline how antibodies help to destroy pathogens.

A

Mark pathogens for destruction:

  1. 2 binding sites mean that antibodies can cause agglutination of the bacterial cells, making it easier for phagocytes to locate them, as not spread out throughout the body.
  2. They then serve as markers, stimulating phagocytes to engulf and destroy the bacterial cells to which the antibodies are attached.
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6
Q

Define monoclonal antibody.

A

= Antibodies produced from a single group of genetically identical B-cells. Monoclonal antibodies are identical in structure.

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7
Q

List uses of monoclonal antibodies.

A
  1. Targeting cancer drugs.
  2. Pregnancy testing.
  3. Diagnosing HIV etc.
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8
Q

Outline how monoclonal antibodies are used in targeting cancer drugs.

A
  1. Monoclonal antibodies can be made that will bind to tumour markers (cancer cell antigens), with anti-cancer drugs attached to antibody.
  2. So, antibodies will bind to tumour markers - drug will only accumulate in areas of body where there are cancer cells.
  3. Therefore, side-effects of an antibody-based drug are lower than other drugs because they accumulate near specific cells.
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9
Q

Outline how monoclonal antibodies are used in pregnancy testing (Medical Diagnosis).

A
  1. Application area contains antibodies for hCG, bound to a blue-coloured bead.
  2. When hCG present in urine, hCG will bind to the antibody on the beads, forming an antigen-antibody complex.

-

  1. Urine moves up the stick to test strip, carrying beads.
  2. Test strip contains immobilised hCG antibodies.
  3. Antibodies bind to hCG if present –> hCG-antibody complex with the blue beads attached becomes more concentrated –> turns blue.
  4. If no hCG present, beads will pass through the test area –> no visible colour change.
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10
Q

Outline how monoclonal antibodies are used in the ELISA test.

A

Enzyme-linked immunosorbent assay:
=> allows us to see if a patient has antibodies for a specific antigen, usually HIV.

Indirect ELISA - used to see if a patient has HIV antibodies.

  1. HIV antigen bound to bottom of a well in a well plate.
  2. Patient’s blood plasma sample (containing antibodies) added to the well. Any HIV-specific antibodies will bind to the antigen in well.
  3. Well washed out to remove any unbound antibodies.
  4. Secondary antibody attached to a specific enzyme which can attach to primary antibody added. Well washed out again to remove unbound secondary antibody.
  5. Solution containing enzyme’s substrate added, which produces a coloured product after the enzyme action.
  6. Colour change of solution —> HIV-specific antibodies present in blood —> infected with HIV.

NB=> Washing steps are crucial!

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11
Q

Explain why the ELISA test does not diagnose AIDS.

A

AIDS is a degenerative disease caused by HIV when T-cell count has declined below a certain level.

Having HIV does not = having AIDS - takes years to develop AIDS.

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12
Q

Outline the ethical issues of monoclonal antibody use.

A
  1. Involves inducing cancer in mice to produce antibodies —> some have reservations, despite guidelines to minimise suffering.
  2. Successfully used to treat many diseases such as cancer and diabetes, BUT some deaths have been associated with their use in MS treatments.
  3. Testing for the safety of new drugs presents new dangers —> 2006 trial, London.

=> Society must weigh up advantages and disadvantages of their use, combined with current scientific knowledge about them to make informed decisions at individual to global levels about the use of drugs such as MAs.

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13
Q

How do vaccines work?

A
  1. Provide protection for individuals and populations against disease.
  2. Vaccination can help avoid suffering caused during the primary immune response.
  3. Vaccines contain antigens that cause the body to produce memory cells against a particular pathogen, without that pathogen causing disease —> immunity without symptoms.
  4. Contain antigens, free or attached to a dead or attenuated (reduced in virulence/weakened) pathogen.
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14
Q

Define herd immunity.

A

= General immunity to a pathogen in a population based on the acquired immunity to it over time by a high proportion of members.

=> less likely to catch a particular disease as less common, as most people are immune.

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15
Q

How and when are vaccines given? Why?

A

Vaccines can be injected or taken orally, but oral vaccines can be broken down/digested by enzymes in GI tract or the vaccine molecules may be too large to be absorbed into the blood.

Sometimes booster vaccines given years after to make sure the memory cells are still produced.

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16
Q

Outline the ethical issues of using vaccines.

A
  1. Often involves use of animals in manufacturing.
  2. Some side-effects may cause long-term harm.
  3. Test them on who? How? To what extent should individuals be asked to accept risk in the interest of public health?
  4. Compulsory? Opt-out? What grounds?
  5. Cost? Should we continue if disease almost eradicated if costly?
17
Q

Define active immunity.

Outline differences between natural active and artificial active immunity.

A

= Immune system making its own antibodies.

a) artificial = becoming immune after being vaccinated against an antigen/disease.
b) natural = becoming immune after catching a disease.

  • requires exposure to antigen.
  • time needed for protection to develop.
  • memory cells produced.
  • long-term protection as memory cells produced -> secondary response possible.
18
Q

Why does vaccination not always eliminate a disease?

A
  1. Antigenic variability, many different varieties.
  2. Some don’t get vaccinated.
  3. Some pathogens ‘hide’ from immune system in cells/intestines etc.
19
Q

Outline/draw the structure of HIV.

A

Include:

  • attachment proteins
  • genetic material (RNA)
  • lipid envelope
  • matrix (outside capsid)
  • capsid
  • reverse transcriptase enzyme
20
Q

Outline how HIV replicates.

A
  1. Enters bloodstream and circulates around the body.
  2. HIV attachment proteins readily bind to CD4 receptor proteins, occurring most frequently on Th-cells.
  3. Protein capsid fuses with cell-surface membrane —> HIV’s RNA and enzymes injected into the Th-cells.
  4. HIV’s reverse transcriptase enzymes convert viral RNA to DNA, which moves to Th-cell nucleus where inserted into cell’s DNA.
  5. Cell’s enzyme used to make mRNA, from viral DNA, passing out through nuclear pores to ribosomes for translation, producing viral RNA and proteins —> new HIV particles.
  6. New HIV particles break away from Th-cell, using a part of the Th-cell-surface membrane to form their lipid envelopes.
21
Q

How does HIV cause the symptoms of AIDS?

A
  1. HIV particles kill/interfere with Th-cell, drastically reducing their numbers in the blood.
  2. Th-cells cannot stimulate B-cells to produce antibodies or the Tc-cells that kill infected cells.

=> body is unable to produce an adequate immune response and becomes susceptible to other infections and cancers.
- secondary diseases ultimately kill the patient; infections of many organs, weight loss and diarrhoea develop.

22
Q

Why are antibiotics ineffective against viruses?

A
  1. Antibiotics like penicillin, inhibit the enzymes required for the synthesis and assembly of the peptide cross-linkages in bacterial cell walls - weakens the walls, making them unable to withstand pressure —> water enters bacterium by osmosis naturally and cell dies.

BUT

  1. Viruses lack their own metabolic pathways and cell structure and rely on those of their host cell:
    - antibiotics are ineffective because there are no metabolic mechanisms or structures for them to disrupt.
  2. Viruses also have a protein coat, not a peptidoglycan murein cell wall —> do not have sites where antibiotics can work.

=> once viruses are within an organism’s own cells, antibiotics cannot reach them.