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the immune system Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

what is an antigen?

A
  • cell surface molecules which trigger sn immune response when detected by our immune system.
  • usually glycoprotein sometimes glycolipid / polysaccharide.
  • immune system recognises as “self” / “nonself” = enables identification of cells from other organisms of same species pathogens , toxins + abnormal body cell.
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2
Q

how does phagocytosis destroy pathogens ?

A

1) detect presence of the pathogen when receptors on its cell surface bind to antigens on pathogen.

2) pathocyte wraps its cytoplasm around pathogen + engulfs it. pathogen contained within type is vesicle : phagosome

3) lysosome (contains digestive enzymes: lysozymes) fuse with phagosome to form phagysosome.

4) lysozymes digest pathogen / destroys it - digested pathogen removed from phagocyte by exocytosis

5) phagocyte absorbs products from pathogen hydrolysis

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3
Q

explain the role of antigen presenting cells .

A
  • macrophage displays antigen from pathogen on its surface (after hydrolysis in phagocytosis)
  • enhances recognition by T(H) cells, which cannot directly interface with pathogens/ antigens in body fluid.
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4
Q

give 2 differences between specific and nonspecific immune responses.

A
  • nonspecific (inflammation, phagocytosis)
    = same for all pathogens
  • specific (B + T lymphocytes) = complementary pathogen
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5
Q

name the 2 types of specific immune system.

A
  • cell-mediated
  • humoral
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6
Q

outline the process of the cell-mediated process

A

1) complementary T lymphocytes bind to foreign antigen on APC

2) release cytokines that stimulate
— clonal expansion of complementary T cells: become memory cells/ trigger humoral response

→ clonal expansion of cytotoxic T cells : secrete enzyme perforin - destroy infected cells

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7
Q

describe T lymphocytes response

A
  • T lymphocytes = WBC contain receptors in their cell surface
  • when particular T cells binds to complementary antigen - T cell become activated (clonal selection)
  • once activated - T cell divides by mitosis to
    produce clones (clonal expansion)
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8
Q

name the different types of T cell which play different roles in immune response .

A
  • Thelper cells - release chemicals (cytokine called interleukins) activate B lymphocytes
  • T killer cells - destroy any cells which have been infected with pathogen
  • Tregulatory cells - suppress other immune cells + prevent them from attacking own (host) cells.
  • T memory cells - remain in bloodstream in low levels in case reinfection occurs —> if antigen detected later they divide into T helper. T killer cells+ T regulatory cells
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9
Q

explain the process of B lymphocytes response .

A
  • B cells activated when chemicals released from Thelper cells - activated when antibody molecules on cell surface bind to complementary antigen
  • diff B cells have diff shaped antibodies on surface - only B cells correct shaped antibodies be activated
  • once activated B cells divide by mitosis + differentiate into: plasma cells + memory cells.
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10
Q

outline the process of humoral response .

A

1) complementary T lymphocytes bind to foreign antigen on antigen-presenting T cells

2) release cytokines that stimulate clonal expansion of complementary ab lymphocytes

3) B cells differentiate into plasma cells

4) plasma cells secrete antibodies with complementary variable region to antigen

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11
Q

what’s the role of plasmas?

A
  • produce antibodies with complementary shape to antigen .
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12
Q

what’s the role of memory cells?

A
  • remain in bloodstream in low levels in case reinfecrion occurs - if detected again
    later date = quickly divide into plasma
    cells
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13
Q

describe the structure of an antibody

A

proteins protect u when unwanted substance enter body

  • quaternary structure - 4 polypeptide chains held by disulphide bridges
  • composed of a variable region - antigen-binding site located . ABS has complementary shape to antigen —> makes specific to that particular antigen
  • constant region - has another binding site —> allows antibody to bind to immune system cells
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14
Q

what’s the role of the hinge region in antibody structure ?

A
  • in between variable region + constant region- provides antibody with flexibility .
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15
Q

how do antibodies lead to destruction of a pathogen?

A
  • formation of antigen-antibody complex results in agglutination, which enhances phagocytosis.
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16
Q

explain the process of agglutination process regarding antibodies destroying pathogens .

A

1) antibodies - 2 antigen-binding sites —> bind to 2 pathogens same time —> pathogen become clumped together
—> phagocytes engulf + digest more pathogens at same time - efficient

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17
Q

explain the process of neutralising toxins = antibodies destroying pathogens

A
  • antibodies bind to toxins which renders them harmless (neutralised them) = antibody-toxin complex can be destroyed by phagocytes.
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18
Q

explain process of blocking access to human cells regarding antibodies destroying pathogens

A
  • pathogens enter host cells when antigens bind receptor molecules on host cells
  • antibodies bind antigens - prevents antigen from fitting in receptor - can’t get inside cell
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19
Q

what’s the difference between cellular vs humoral immune response ?

A
  • cellular immune response - includes phagocytosis and T-cell response
  • humoral immune response - includes B-cells and antibodies they produce
20
Q

describe what is meant by primary immune response.

A
  • when u are infected with pathogen for first time . composed: non-specific + specific immune response
21
Q

why is the process of primary immune response slow ?

A
  • takes time for correct B cell to be activated + divide into lots plasma cells to produce antibodies with complementary shape to antigen .
  • both T and B cells produce memory cells
22
Q

explain the secondary immune response.

A
  • re infected with same pathogen in future - T and B memory cells recognise antigen + starts dividing
  • T memz cells divides to correct type T killer cell to kill cells that’s infected with pathogen
  • B memz cells divide to plasma cells —> produce large no. antibodies : complementary to antigen molecules on pathogen
23
Q

define the term vaccine.

A
  • contains dead or weakened form of a pathogen which injected into the bloodstream
24
Q

what does the injection of weakened antigens stimulate ?

A
  • primary immune response + production of memz T cells + memz B cells —> results immunity without being ill from disease
25
Q

what causes antigen variability ?

A

1) random genetic mutation changes DNA base sequence

2) results in diff sequence of codons on mRNA

3) diff primary structure of antigen = H-bonds, ionic bonds + disulphide bridges form in diff places in tertiary structure

4) diff shape of antigen

26
Q

explain how antigen variability affects the incidence of disease

A
  • memory cells no longer complementary to antigen = individual not immune = can catch disease more than once
  • many varieties of a pathogen = difficult to develop vaccine containing all antigen types
27
Q

describe what’s meant by active immunity .

A
  • when ur body makes its own antibodies after being stimulated by an antigen .
  • natural process or artificial
  • natural = humoral response to infection
  • artificial = vaccination
28
Q

describe what’s meant by the term passive immunity .

A
  • occurs when you given ready-made antibodies that’s been produced by another organism
  • natural = antibodies in breast milk/ across placenta
  • artificial = anti-venom, needle stick injections .
29
Q

contrast passive and active immunity.

A

PASSIVE .
- no memz cells + antibodies not replaced when broken down = short term
- short-lived
- immediate protection against pathogens
- antibodies from external source
- direct contact with antigen not necessary

ACTIVE
- memz cells produced = long-term
- time lag
- lymphocytes produce antibodies
- direct contact with antigen necessary

30
Q

explain the principles of vaccination.

A

1) vaccine contains dead/inactive form of a pathogen/antigen

2) triggers primary immune response

3) memz cells produced + remain in bloodstream so secondary response is rapid + produces higher conc of antibodies

4) pathogen destroyed before it causes symptoms .

31
Q

what is herd immunity ?

A
  • vaccinating large proportion of population reduces available carriers of the pathogens
  • protects individuals who haven’t been vaccinated (those with weak immune system)
32
Q

suggest some ethical issues surrounding the use of vaccines

A
  • production may involve use of animals
  • potentionally dangerous side-effect
  • clinical tests may be fatal
  • compulsory vs opt-out
33
Q

what are monoclonal antibodies ?

A
  • antibodies produced from a single clones of B cells so have exact same structure .
  • can be developed to bind to anything, not js antigens but pathogens
34
Q

describe how monoclonal antibodies used in pregnancy tests

A
  • there’s antibodies for human chorionic gonadotropin (hCG) hormone .
    —> hCG hormone released by foetuses —> found in urine of preggo - antibodies = blue bead
  • if there’s hCG present in urine - bind to antibody on beads
  • urine moves up stick to test strip —> test trip contains immobilised hCG antibodies (fixed in position on test strip)
  • if hCG present = immobilised antibodies bind hormone that’s attached mobile hCG antibody + blue bead —> cause strip turn blue is hormone present
  • if hCG present A beads pass through test area without binding anything so test strip white
35
Q

explain the purpose of the ELISA test

A
  • (enzyme- linked immunosorbent assay)
  • used in medical diagnosis to see if someone has antibodies against a certain pathogen
  • 2 types: direct ELISA + direct ELISA
36
Q

explain the principle of the a direct ELISA test.

A
  • detects presence of a specific antigen

1) monoclonal antibodies bind to bottom of test plate

2) antigen molecules in sample bind to antibody - rinse excess.

3) mobile antibody with “reporter enzyme” attached binds to antigen that’s “fixed” on monoclonal antibodies == rinse excess

4) add substrate for reporter enzyme - positive result– colour change

37
Q

explain the principles of an indirect ELISA test.

A
  • detects presence of an antibody against a specific antigen .

1) antigens bind to bottom of test plate.

2) antibodies in sample bind to antigen . wash away excess

3) secondary antibody with “reporter enzyme” attached binds to primary antibodies from sample

4) add substrate for reporter enzyme . positive result = colour change

38
Q

suggest clinical application of monoclonal antibodies .

A
  • pregnancy tests by detecting HCG hormones in urine
  • diagnostic procedures ELISA
  • targeted treatment = attaching drug to antibody so can only bind to cells with abnormal antigen.
39
Q

suggest some ethical issues surrounding use of monoclonal antibodies .

A
  • production involves animals
  • drug trails against arthritis + leukaemia resulted in multiple organ failure .
40
Q

what’s meant by HIV (human immunodeficiency virus )

A
  • deadly virus which can weaken a persons immune system by destroying type of immune cell called T helper cells
  • spread through transmission of infected bodily fluids.
41
Q

what does opportunistic infection refer to?

A
  • weakens the immune system to extent patient unable fight off other infections which normally not pose threat.
42
Q

describe the structure of HIV

A
  • genetic material ( 2 x RNA) + viral enzymes (integrate + reverse transcriptase) surrounded by capsid
  • surrounding capsid is outer layer called envelope derived from host cell membrane
  • GP120 attachment proteins on surface (for virus to enter host cells )
43
Q

how does HIV result in symptoms of AIDS?

A

1) attachment proteins bind to complementary CD4 receptor on T cells

2) HIV particles replicate inside T cells , killing / damaging them

3) AIDS develops when there’s few T cells for immune system to function

4) individuals cannot destroy other pathogens + suffer from secondary diseases

44
Q

what are the symptoms of stages of AIDS

A

1) person first develop less serious, minor infection —> gradually become more severe

2) as patients body tries to fight off more infections: the lower their T cells levels drop

3) eventually immune system be weak - die of an opportunistic infection as don’t have enough immune cells to defend themselves .

45
Q

explain process if person has HIV

A

1) person with hiv exchanges bodily fluid with another person- can infect second person

2) HIV virus uses its attachment proteins to enter human immune cells by binding to receptors on T cell.

3) capsid released into cell , breaks apart to release RNA and enzymes

4) enzyme reverse transcriptase converts RNA into DNA - enzymes integrase insert into DNA of T cells.

5) viral DNA transcribes + translated + viral proteins used to build new virus particles - move out of T cell + infect other cells.

46
Q

how do antibiotics work?

A
  • interfering with bacterial cell walls/ribosomes (killing bacteria or stopping growth ) no effect on viruses / own cells as
  • viruses not have ribosomes/cell walls = antibiotic treatment is ineffective against viral infections
  • human cells don’t have cell walls = bigger ribosomes than those found in bacteria + unaffected by antibiotics .
    —> useful = fake antibiotics without worrying abt it interfering with own cells .
47
Q

why are antibiotics ineffective against viruses ?

A
  • antibiotics often work by damaging murein cells walls to cause osmotic lysis = viruses have no cell wall
  • viruses replicate inside host cells = hard to destroy them without damaging normal body cells

BIOLOGY (14 decks)

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