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A Level Biology > Cell Recognition and the Immune System > Flashcards

Cell Recognition and the Immune System Flashcards

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1
Q

what is an antigen

A

-a foreign molecule/protein
-that stimulates an immune response
-leading to the production of antibodies

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2
Q

how are cells identified by the immune system

A

-each cell has specific molecules on its surface that identify it
-these molecules are often proteins with a specific tertiary structure

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3
Q

what types of cells and molecules can the immune system identify

A

-pathogens
-cells from other organisms of the same species
-abnormal body cells
-toxins released by some bacteria

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4
Q

what is a pathogen

A

-a disease causing microorganism

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5
Q

describe phagocytosis of pathogens (non specific immune response)

A

-phagocyte is attracted to chemoattractants from pathogen/ recognises antigens on pathogen
-phagocyte engulfs pathogen by surrounding it with its cell membrane
-pathogen contained in vesicle/phagosome in cytoplasm of phagocyte
-lysosome fuses with phagosome and releases lysozymes
-lysozymes hydrolyse pathogen
-phagocytes absorb products of hydrolysis

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6
Q

what does phagocytosis lead to

A

-presentation of antigens on the phagocyte cell surface membrane
-stimulating the specific immune response

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7
Q

describe the response of t lymphocytes to a foreign antigen (the cellular response)

A

-t lymphocytes recognise antigen presenting cells
-specific helper T cells with complementary receptors bind to antigen on the antigen presenting cell
-the antigen presenting cell is activated and divides by mitosis to form clones

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8
Q

what do the clones produced in the t lymphocyte response stimulate

A

-cytotoxic cells which kill infected cells
-specific b cells
-phagocytes

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9
Q

describe the response of b lymphocytes to a foreign antigen (humoral response)

A

-specific b lymphocyte with complementary receptor binds to antigen
-this is stimulated by helper T cells which releases cytokines
-so divides rapidly by mitosis to form clones (clonal selection)
-differentiate into b plasma or b memory cells

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10
Q

what can b lymphocytes recognise

A

-free antigens, not just antigen presenting cels

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11
Q

what do b plasma cells do

A

-secrete large amounts of antibodies

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12
Q

what do b memory cells do

A

-remain in the blood for the secondary immune response

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13
Q

what are antibodies

A

-quaternary structure proteins
-secreted by b lymphocytes in response to specific antigens
-bind specifically to antigens forming antigen-antibody complexes

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14
Q

describe the structure of an antibody

A

-variable region
-constant region
-heavy polypeptide chain
-light polypeptide chain
-antigen binding site
-hinge region
-disulfide bridge

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15
Q

explain how antibodies lead to the destruction of pathogens

A

-antibodies bind to antigens on pathogens forming an antigen-antibody complex
-as they have a specific tertiary structure so the binding site is complementary to the antigen
-each antibody binds to 2 pathogens at a time causing agglutination of pathogens
-antibodies attract phagocytes
-phagocytes bind to the antibodies and phagocytose many pathogens at once

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16
Q

describe the primary immune response

A

-first exposure to antigen
-antibodies produced slowly and at a lower concentration
-takes time for specific b plasma cells to be stimulated to produce specific antibodies
-memory cells are produced

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17
Q

describe the secondary immune response

A

-second exposure to antigen
-antibodies produced faster and at a higher concentration
-b memory cells rapidly undergo mitosis to produce many plasma cells which produce specific antibodies

18
Q

what is a vaccine

A

-injection of antigens from attenuated pathogens
-stimulating formation of memory cells

19
Q

explain how vaccines provide protection to individuals against disease

A

-specific b lymphocyte with complementary receptor binds to antigen
-specific t helper cell binds to antigen presenting cell and stimulates b cell
-b lymphocyte divides by mitosis to form clones
-some differentiate into b plasma cells which release antibodies
-some differentiate into b memory cells
-on second exposure to antigen, b memory cells divide rapidly by mitosis to produce b plasma cells
-these release antibodies faster and at a higher concentration

20
Q

explain how vaccines provide protections for populations against disease

A

-herd immunity
as
-large proportion of population immune so don’t become ill from infection
-fewer infected people pass pathogen on/unvaccinated people less likely to come into contact with someone with the disease

21
Q

what is herd immunity

A

-large proportion of population vaccinated, reducing spread of pathogen

22
Q

describe active immunity

A

-initial exposure to antigen
-memory cells involved
-antibody produced and secreted by b plasma cells
-slow, takes longer to develop
-long term immunity as antibody can be produced in response to a specific antigen again

23
Q

describe passive immunity

A

-no exposure to antigen
-no memory cells involved
-antibody introduced from another organism eg breast milk/placenta
-faster acting
-short term immunity as antibody hydrolysed

24
Q

explain the effect of antigen variability on disease and disease prevention

A

-antigens on pathogens change shape/tertiary structure due to gene mutations (creating new strains)
-so no longer immune
-b memory cell receptors cannot bind to changed antigen on secondary exposure
-specific antibodies not complementary to changed antigen

25
Q

examples of antigen variability affecting diseases

A

-yearly flu vaccinations developed
-no vaccine for HIV
-can catch a cold many times

26
Q

describe the structure of a HIV particle

A

-lipid envelope
-RNA
-reverse transcriptase
-capsid
-attachment protein

27
Q

describe the replication of HIV in helper T cells

A

-HIV attachment proteins attach to the receptors on helper T cell
-lipid envelope fuses with cell surface membrane, releasing capsid into cell
-capsid uncoats, releasing RNA and reverse transcriptase
-reverse transcriptase converts viral RNA to DNA
-viral DNA inserted/ incorporated into helper T cell DNA (may remain latent)
-viral protein/capsid/enzymes are produced
a) DNA transcribed into HIV mRNA
b) HIV mRNA translated into new HIV proteins
-virus particles assembled and released from cell (via budding)

28
Q

explain how HIV causes the symptoms of AIDS

A

-HIV infects and kills helper T cells (host cell) as it multiplies rapidly
-so T helper cells cant stimulate cytotoxic T cells, B cells and phagocytes
-so B plasma cells can’t release as many antibodies for agglutination and destruction of pathogens
-immune system deteriorates so more susceptible to infections
-pathogens reproduce, release toxins and damage cells

29
Q

explain why antibiotics are ineffective against viruses

A

viruses do not have structures/ processes that antibiotics inhibit:
-viruses do not have metabolic processes eg do not make protein/ribosomes
-viruses do not have bacterial enzymes/murein cell wall

30
Q

what is a monoclonal antibody

A

-antibody produced from genetically identical/cloned B lymphocytes/plasma cells
-so have same tertiary structure

31
Q

explain how monoclonal antibodies can be used in medical treatments

A

-monoclonal antibody has a specific tertiary structure/variable region
-complementary to receptor/protein/antigen found only on a specific cell type
-therapeutic drug attached to antibody
-antibody binds to specific cell, forming antigen-antibody complex, delivering drug

32
Q

what are some monoclonal antibodies designed to do other than being attached to a therapeutic drug

A

-block antigens/receptors on cells

33
Q

explain how monoclonal antibodies can be used in medical diagnosis

A

-monoclonal antibody has a specific tertiary structure/variable region
-complementary to specific receptor/protein/antigen associated with diagnosis
-dye/stain/fluorescent marker attached to antibody
-antibody binds to receptor forming antigen-antibody complex

34
Q

explain the use of antibodies in the ELISA test to detect antigens (direct)

A

-attach sample with potential antigens to well
-add complementary monoclonal antibodies with enzymes attached that will bind to antigens if present
-wash well to remove unbound antibodies that could cause a fake positive
-add substrate - enzymes create products that cause a colour change (positive result)

35
Q

explain the use of antibodies in the ELISA test to detect antigens (sandwich)

A

-attach specific monoclonal antibodies to well
-add sample with potential antigens, then wash well
-add complementary monoclonal antibodies with enzymes attaches which bind to antigens if present
-wash well to remove unbound antibodies that could cause a false positive
-add substrate - enzymes create products that cause a colour change

36
Q

explain the use of antibodies in the ELISA test to detect antibodies (indirect)

A

-attach specific antigens to well
-add sample with potential antibodies, wash well
-add complementary monoclonal antibodies with enzyme attached which bind to antibodies if present
-wash well to remove unbound antibodies
-add substrate as enzymes create products that cause a colour change

37
Q

suggest the purpose of a control well in the ELISA test

A

-compare to test to show only enzyme causes colour change
-compare to test to show all unbound antibodies have been washed away

38
Q

suggest why failure to thoroughly wash the well can result in a false positive on the ELISA test

A

-antibody with enzyme remains/not washed out
-so substrate converted into colour product

39
Q

discuss some general ethical issues associates with the use of vaccines and monoclonal antibodies

A

-pre clinical testing on/ use of animals - potential harm/stress
but animals not killed and helps produce drugs to reduce human suffering
-clinical trials on humans - potential harm/side effects
-vaccines - may continue high risk activities and still develop/pass on pathogen
-use of drug- potentially dangerous side effects

40
Q

suggest some points to consider when evaluating methodology relating to the use of vaccines and monoclonal antibodies

A

-was the sample size large enough to be representative
-were participants diverse in terms of age, sex, ethnicity and health
-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

41
Q

what is a double blind trial

A

-neither doctor/patient knew who was given drug or placebo

42
Q

suggest some points to consider when evaluating evidence and data relating to the use of vaccines and monoclonal antibodies

A

-what side effects observed and how frequently
-was a statistical test used - difference in start and final results
-was the standard deviation of final results large
-did standard deviations of start and final results overlap
-what dosage was optimum
-does increasing dose increase effectiveness enough to justify extra cost
-was the cost of production and distribution low enough

A Level Biology (18 decks)

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