Cell recognition & the immune system Flashcards

1
Q

What is an antigen?

A

a foreign molecule (protein) that stimulates an immune response which leads to the production of antibodies

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2
Q

How are cells identified by the immune system?

A
  • each type of cell has specific molecules on its surface that identify it
  • they’re often proteins which have a specific tertiary structure
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3
Q

What types of cells & molecules can the immune system identify?

A
  • pathogens e.g. viruses, bacteria, fungi
  • cells from other organisms of the same species e.g. organ transplants
  • abnormal body cells e.g. tumour cells
  • toxins released from bacteria
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4
Q

What are the steps of phagocytosis of pathogens?

A
  1. phagocyte recognises foreign antigens on pathogen
  2. phagocyte engulfs pathogen by surrounding it with its cell membrane
  3. pathogen contained in vesicle (phagosome) in cytoplasm
  4. lysosome fuses with phagosome & releases lysozymes which are hydrolytic enzymes
  5. lysozymes hydrolyse pathogens
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5
Q

What does phagocytosis lead to?

A

the presentation of antigens displaced on the phagocyte cell-surface membrane which stimulates the specific immune response

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6
Q

What is the function of T lymphocytes?

A

to recognise antigen presenting cells e.g. infected cells, phagocytes presenting antigens, transplanted cells, tumour cells etc.

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7
Q

What is the response of T lymphocytes to a foreign antigen cellular response) ?

A
  • specific helper T cells with complementary receptors bind to antigen on antigen-presenting cell which activates its division by mitosis to form clones
    -the clones stimulate:
  • cytotoxic T cells - kill infected cells by producing perforin
  • specific B cells - involve humoral response
  • phagocytes - engulf pathogens by phagocytosis
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8
Q

What is the function of B lymphocytes?

A

they can recognise free antigens in body fluids e.g. blood

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9
Q

What is the response of B lymphocytes to a foreign antigen (humoral response) ?

A
  1. clonal selection:
    - specific B lymphocyte with complementary receptor binds to antigen
    - this is stimulated by helper T cells so divides by mitosis to form clones
  2. some differentiate into B plasma cells which secrete monoclonal antibodies
  3. some differentiate into B memory cells which remain in blood for secondary immune response
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10
Q

What are antibodies?

A

quaternary structure proteins secreted by B lymphocytes which specifically bind to antigens forming antigen-antibody complexes

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11
Q

What are the components that make up the structure of an antibody?

A
  • antigen
  • antigen binding site
  • disulfide bridge
  • variable region
  • constant region
  • light & heavy polypeptide chain
  • hinge region
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12
Q

How do antibodies lead to the destruction of pathogens?

A
  • antibodies bind to pathogens forming antigen-antibody complex - they have a specific tertiary structure so binding site is complementary to antigen
  • each antibody binds to 2 pathogens at a time causing agglutination of pathogens
  • antibodies attract phagocytes
  • phagocytes bind to antibodies & phagocytose many pathogens at once
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13
Q

What are the differences between the primary & secondary immune response?

A

primary - first exposure to antigen:
- antibodies produced slowly at a lower conc
- takes time for specific B plasma cells to be stimulated to produce specific antibodies
- memory cells are produced
secondary - second exposure to antigen
- antibodies produced faster at a higher conc
- B memory cells rapidly undergo mitosis to produce many plasma cells which produce specific antibodies

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14
Q

What is a vaccine?

A

an injection of antigens from dead or weakened pathogens which stimulates formation of memory cells

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15
Q

How do vaccines provide protection to individuals against disease?

A
  1. specific B lymphocyte with complementary receptor binds to antigen
  2. specific T helper cell binds to antigen-presenting cell & stimulates B cell
  3. B lymphocyte divides by mitosis to form clones
  4. Some B cells differentiate into B plasma cells which release antibodies
  5. others differentiate into B memory cells
  6. on secondary exposure to antigen B memory cells divide by mitosis rapidly to produce B plasma cells
  7. B plasma cells secrete antibodies faster & at a higher conc
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16
Q

How do vaccines provide protections for populations against disease?

A
  • herd immunity - large proportion of population is vaccinated which reduces spread of pathogen
  • large proportion of population is immune so don’t become ill from infection
  • fewer infected people pass pathogen on
  • unvaccinated people are less likely to come in contact with someone with the disease
17
Q

What are the differences between active & passive immunity?

A
  • initial exposure to antigen in active immunity & no exposure to antigen in passive
  • memory cells are involved in active immunity & aren’t in passive
  • antibody produced & secreted from B plasma cells in active immunity but in passive immunity antibody is introduced from another organism e.g. breast milk
  • active immunity is slow & takes longer to develop whilst passive immunity is faster acting
  • active immunity is long term as antibody can be produced again in response to specific antigen but passive immunity is short term as antibody is hydrolysed
18
Q

What is the effect of antigen variability on disease & disease prevention?

A
  • antigens on pathogens can change shape due to genetic mutations which creates new strains
  • body is no longer immune from vaccine
  • B memory cell receptors can’t bind to changed antigen on secondary exposure
  • specific antibodies aren’t complementary to changed antigen
19
Q

What is the structure of a HIV particle?

A
  • lipid envelope
  • RNA
  • reverse transcriptase
  • capsid
  • attachment protein
20
Q

What is the process of HIV replication in helper T cells?

A
  1. HIV attachment proteins attach to receptors on helper T cell
  2. lipid envelope fuses with cell-surface membrane releasing capsid into cell
  3. capsid uncoats releasing RNA & reverse transcriptase
  4. reverse transcriptase converts viral RNA to DNA
  5. viral DNA inserted into helper T cell DNA
  6. Viral proteins are produced - DNA is transcribed into HIV mRNA which is translated into HIV proteins
  7. virus particles assemble & are released from the cell by budding
21
Q

How does HIV cause the symptoms of AIDS?

A
  • HIV infects & kills T Helper cells - so cytotoxic T cells, B cells & phagocytes aren’t stimulated
  • immune system deteriorates - more susceptible to infections
  • pathogens reproduce, release toxins & damage cells
22
Q

Why are antibiotics ineffective against viruses?

A
  • viruses don’t have metabolic processes
  • viruses don’t have murein cell wall like bacteria
23
Q

What is a monoclonal antibody?

A

antibody produced from genetically identical B plasma cells with the same tertiary structure

24
Q

How are monoclonal antibodies used in medical treatments?

A
  • they have a specific binding site which is complementary to an antigen found on a specific cell type
  • therapeutic drug is attached to the antibody
  • antibody binds to specific cell forming antigen-antibody complex and delivers the drug
25
How can monoclonal antibodies be used in medical diagnosis?
- they have a specific binding site which is complementary to an antigen associated with the diagnosis - a dye is attached to the antibody - antibody binds antigen forming antigen-antibody complex
26
What is the use of antibodies in the ELISA test to detect antigens (direct ELISA) ?
1. attach sample to potential antigens to well 2. add complementary monoclonal antibodies with enzymes attached - they will bind to antigens if present 3. wash well to remove unbound antibodies (prevents false + test) 4. add substrate - enzymes create products that causes colour change which indicates positive result
26
What is the use of antibodies in the ELISA test to detect antigens (sandwich ELISA) ?
1. attach specific monoclonal antibodies to well 2. add sample with potential antigens then wash well 3. add complementary monoclonal antibodies with enzymes attached - binds to antigens if present 4. wash well to remove unbound antibodies to prevent false + test 5. add substrate - enzymes create product that causes colour change showing + result
27
What is the use of antibodies in the ELISA test to detect antibodies?
1. attach specific antigens to well 2. add sample with potential antibodies & wash well 3. add complementary monoclonal antibodies with enzymes attached which binds to antibodies if present 4. wash well to remove unbound antibodies 5. add substrate - enzymes create products that cause colour change showing + result
28
What is the purpose of a control well in the ELISA test?
- compare to test to show only enzyme causes colour change - compare to test to show all unbound antibodies have been washed away
29
Why is failure to thoroughly wash the well results in a false positive in the ELISA test?
- antibody with enzyme remains in the well - substrate converted into colour product
30
What are some general ethical issues associated with the use of vaccines & monoclonal antibodies?
- use on animals - potential stress, harm & mistreatment - but animals aren't killed but help produce new drugs to reduce human suffering - clinical trials on humans - potential harm & side effects - vaccines - may continue high risk activities & still develop/ pass on pathogen - use of drug - potentially dangerous side effects
31
What are some points to consider when evaluating methodology relating to the use of vaccines & monoclonal antibodies?
- was the sample size large enough to be representative? - were pps diverse in terms of age, sex, ethnicity & health status? - were placebo/ control groups used for comparison?- was the duration of the study long enough to show long-term effects? - was the trial double-blind to reduce bias?
32
What are some points to consider when evaluating evidence & data relating to the use of vaccines & monoclonal antibodies?
- what side effects were observed & how frequently did they occur? - was a statistical test used to see if there was a significant difference between start & final results? - was the standard deviation of final results large, showing some people did not benefit? - did standard deviations of stat & final results overlap, showing there may not be a significant difference? - what dosage was optimum? does increasing dose increase effectiveness enough to justify extra cost? - was the cost of production & distribution low enough?