2.4 Cell Recognition and the Immune System Flashcards

(42 cards)

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
examples of antigen variability affecting diseases
-yearly flu vaccinations developed -no vaccine for HIV -can catch a cold many times
26
describe the structure of a HIV particle
-lipid envelope -RNA -reverse transcriptase -capsid -attachment protein
27
describe the replication of HIV in helper T cells
-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
explain how HIV causes the symptoms of AIDS
-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
explain why antibiotics are ineffective against viruses
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
what is a monoclonal antibody
-antibody produced from genetically identical/cloned B lymphocytes/plasma cells -so have same tertiary structure
31
explain how monoclonal antibodies can be used in medical treatments
-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
what are some monoclonal antibodies designed to do other than being attached to a therapeutic drug
-block antigens/receptors on cells
33
explain how monoclonal antibodies can be used in medical diagnosis
-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
explain the use of antibodies in the ELISA test to detect antigens (direct)
-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
explain the use of antibodies in the ELISA test to detect antigens (sandwich)
-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
explain the use of antibodies in the ELISA test to detect antibodies (indirect)
-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
suggest 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
38
suggest why failure to thoroughly wash the well can result in a false positive on the ELISA test
-antibody with enzyme remains/not washed out -so substrate converted into colour product
39
discuss some general ethical issues associates with the use of vaccines and monoclonal antibodies
-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
suggest some points to consider when evaluating methodology relating to the use of vaccines and monoclonal antibodies
-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
what is a double blind trial
-neither doctor/patient knew who was given drug or placebo
42
suggest some points to consider when evaluating evidence and data relating to the use of vaccines and monoclonal antibodies
-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