2.4 Immune system Flashcards

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1
Q

describe how a pathogen can be destroyed by phagocytosis in the body (5)

A
  1. phagocyte attracted by chemo-attractants released by pathogen
  2. phagocyte engulfs pathogen enclosing it in a vesicle called phagosome
  3. lysosome membrane fuses with phagosome membrane
  4. lysosome contains hydrolytic enzymes called lysozymes -> released into phagosome
  5. enzymes hydrolyse the molecules that the pathogen is made of
  6. soluble molecule eg. amino acids and glucose absorbed into the cytoplasm of phagocyte
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2
Q

What is an antigen

A

A foreign protein or glycoprotein (often found on the surface of a cell) which stimulates an immune response

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3
Q

What is a toxin

A

A poison produced by a living organism

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4
Q

A pathogen is

A

a disease causing agent

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5
Q

What organisms do nonspecific immune responses target

A
  • toxins
  • foreign cells / cells from other organisms of the same species
  • abnormal cells (damage / cancerous)
  • pathogens
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6
Q

Why do we need antigen presenting cells?

A

T cells will only respond to antigens that are attached to an antigen presenting cell rather than to antigens on the pathogen / within the body’s fluid

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7
Q

With reference to the immune system, explain the importance of cell to cell recognition

A
  • To recognise pathogens so that T helper cells / phagocytes can be activated
  • To detect the presence of abnormal / cancer cells so that they can be destroyed by T helper cells
  • Ability to recognise self and non self cells and molecules so non self cells can be targeted by B lymphocytes
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8
Q

describe what happens after phagocytosis of a pathogen (regarding T cells)

A
  • once phagocyte engulfs pathogen ➜ can display pathogen’s antigens on its cell surface membrane
  • phagocyte acts as an APC
  • T cells w/ receptors complimentary to a specific antigen binds to the APC
  • T cells become activated
  • these divide by mitosis to make many more Tₕ cells
  • also produce chemicals
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9
Q

T cell clonal selection definition

A
  • activation of a specific T cell that has receptors that are complimentary to a specific antigen
  • this T cell divides by mitosis to produce genetically identical T cells (clones)
  • (same happens for Tₕ and Tc cells)
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10
Q

4 things that a Tₕ cell can do :

A
  1. stimulate B cells
  2. stimulate cytotoxic T cells
  3. stimulate phagocytosis
  4. Th cells become T memory cells
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11
Q

how are cytotoxic T cells activated by Tₕ cells (2)

A
  • cytotoxic T cells also have receptors on their cell surface membrane
  • can be activated by binding to the APC together with chemical secreted by Tₕ cells
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12
Q

how do Tc cells kill APC’s

A
  • Tc cells produce proteins (perforin) ➜ can make the APC’s membrane permeable ➜ can kill cell
  • holes allow toxins to get in, will deffo kill the cell and everything in it (eg. viruses that have invaded cell)
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13
Q

how can the body quickly respond to the same pathogen invading again?

A
  • some Tₕ cells that had receptors complimentary to specific antigen on pathogen stay in blood after infection has passed
  • Th cells become T memory cells
  • helps body respond quicly if it encounters the same pathogen again
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14
Q

Describe the cell mediated immune response and the role of different T cells (6)

A

Phagocyte engulfs pathogen
phagocyte presents antigens on its cell surface membrane becoming an antigen presenting cell
* helper T cells with receptors complementary to the specific antigen bind to the APC
* T helper cells become activated
* Th cells divided by mitosis
* activated TH cells secrete cytokines which activate other T cells called cytotoxic T cells
* t cells activate specific B cells which have receptors complementary to the same antigen
* t cells can also stimulate phagocytosis
* t cells become T memory cells

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15
Q

The specificity of an antibody depends on its variable regions how? (2)

A
  • variable regions have specific tertiary and primary structures
  • creates a complimentary binding site to one specific antigen
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16
Q

how does antibody-antigen complexes help you not get harmed by pathogens

A

agglutination: clumping together of antigen bearing cells in the prescence of their complimentary antigen
* antibody binding to antigen also attracts phagocytes

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17
Q

Non self cells….

A

Stimulate an immune response

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18
Q

Vaccine definition

A

A vaccine contains an antigen, or several, from a pathogen that stimulates an immune response, resulting in formation of memory cells

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19
Q

Immunity definition

A

Ability of an organism to resist a particular infection (or toxin) by the action of the specific immune response

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20
Q

Explain why this antibody will only detect one antigen: (4)

A
  • antigen has specific primary structure
  • antibody has a certain tertiary structure that forms the binding site
  • that is complementary to a specific antigen
  • forming an antibody antigen complex
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21
Q

what should be checked during making a vaccine (4)

A
  • dose to be given
  • no serious side effects
  • how effective
  • cost of drug
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22
Q

monoclonal antibody definition

A

antibodies with the same tertiary structure prod. by clones of a specific B plasma cell

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23
Q

Describe how antibodies are produced in the body following a viral infection. (6)

A
  • The virus has an antigen on its surface.
  • The virus is engulfed by a phagocyte.
  • The phagocyte presents the antigen to the B cell.
  • Memory cells and B cells are activated
  • And they divide by mitosis to form clones.
  • Plasma cells release antibodies.
  • Antibodies are specific to an antigen.
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24
Q

Explain how changes in numbers of Golgi body. Mitochondria and RER is related to the function of B lymphocytes.

A
  • More GOLGI BODY to PACKAGE more PROTEINS for SECRETION.
  • MORE MITOCHONDRIA provide more ATP.
  • MORE RER so that RIBOSOMES can SYNTHESISE PROTEINS.
  • ALL OF THESE FUNCTIONS ALLOW THE B LYMPHOCYTES TO PRODUCE ANTIBODIES.
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25
Q

Explain how antigenic variability has caused some people to become infected with a virus more than once. (2)

A
  • Antigens can change so they aren’t recognised by MEMORY CELLS.
  • A primary response is triggered again. This takes LONG TO PRODUCE & RELEASE ANTIBODIES.
26
Q

Give two ways in which passive immunity differs from active immunity.

A
  1. Active immunity produces antibodies.
  2. Passive immunity is shorter lived.
  3. No memory cells produced with passive immunity.
27
Q

B lymphocytes can respond to

A

antigens in the body’s fluid or on CSM

28
Q

Why might one type of pathogen cause the activation of more than one type of B cell? (2)

A
  • all cells have more than 1 type of antigen on their surface
  • b cells can also be activated by toxins produced by pathogens
29
Q

Why is the primary response slow and produces less antibodies

A

It takes time for:

  • clonal selection to occur to identify the helper T cells with the receptors complementary to the specific antigens present
  • clonal selection to occur to identify the B cells with the antibodies complementary to the specific antigens present
  • B cells to be activated by t helper cells and divide by mitosis
  • b plasma cells to produce antibodies
30
Q

If a sheep is injected with the box jellyfish venom on more than one occasion a higher yield of antivenom is obtained. Explain why (3)

A
  • B cells specific to the venom divide by mitosis
  • B cells produce plasma cells and memory cells
  • The second dose produces antibodies in secondary immune response in higher concentration and quickly
31
Q

What is antigenic variability?

A
  • if a pathogen has antigenic variability, the genes which code for the antigen proteins mutate from one generation to the next
  • different antigens on cell surface
  • so the antigen changes from one generation to the next
32
Q

What are the consequences for an organism who re-encounters a pathogen with conserved variability? (3)

A
  • receptors and antibodies from B memory cells are complementary to the antigens
  • secondary immune response is faster
  • pathogen is destroyed
  • no symptoms
33
Q

Why do we only get chicken pox once but we can get flu many times?

A

Chicken pox

  • antigens are conserved from one generation to the next
  • secondary infection is recognised by complementary receptors on b memory cells
  • secondary immune response is fast so destroys pathogens before symptoms are felt

Flu

  • has antigenic variability so antigens mutate from one generation to the next
  • change in specific tertiary structure of antigen
  • antigen is no longer complementary to memory B cells’ receptors so it can no longer bind
  • primary immune response is slow so symptoms are felt
34
Q

Define immunity

A

The ability of an organism to resist a particular infection by the action of the specific immune response

35
Q

Passive immunity

A
  • antibodies are produced from another source
  • bind to the antigen
  • cause agglutination

(E.g. from mother to child through breast milk, antibodies given via injection, anti venom for snake bites)

  • immediate protection
  • short lived
36
Q

Active immunity definition and its qualities. (3)

A
  • when the antigens enter the body and the body produces its own T cells, b cells and antibodies

E.g. immune response to a vaccine

  • takes time to develop
  • long lasting immunity
37
Q

What is the ELISA test used for

A

uses antibodies to detect the presence and quantity of an antigen in a sample and vice versa

38
Q

Describe how antibodies could be used to detect the presence of antibodies (ELISA HIV test)

A
  1. the first antibody binds to the antigen

(plate is washed)

  1. the second antibody with an enzyme attached is added
  2. the second antibody binds to the antigen

(plate is washed to remove unbound antibodies)

  1. a colorless substrate is added
  2. changes color if positive result
39
Q

The percentage of the population vaccinated does not need to be 100 % to be effective in preventing the spread of whooping cough. Suggest why? (2)

A
  • more people are immune so fewer people to carry pathogen
  • susceptible hosts less likely to come into contact with infected individuals
40
Q

Explain why HSV only infects nerve cells (3)

A
  • virus has attatchment proteins on its cell surface membrane
  • with complimentary shape to receptor in membrane
  • receptor only found on nerve cell membrane
41
Q

Scientists have found that microDNA from HSV bind to cell’s mRNA (which are responsible for programmed cell death of nerve cells), allowing it to stay in the body for years.

A

MicroRNA binds to cell’s mRNA
1. (Binds) by specific base pairing;
2. (So) prevents mRNA being read by/ binding to ribosomes;
3. (So) prevents translation / production of proteins;
4. (Proteins) that cause cell death.
thr4, the nerve cells that are infected with HSV don’t die

42
Q

What enzyme do viruses contain?

A

reverse transcriptase

43
Q

List the structures of virus: (5)

A
  • attatchement protein
  • capsid
  • lipid envelope
  • single stranded RNA
  • enzymes
44
Q

Describe how a vaccine leads to antibody production against a pathogen. (6)

A
  • Vaccine contains antigen of pathogen
  • Phagocyte presents antigen on cell surface membrane
  • T helper cells with complimentary receptor protein bind to antigen
  • T helper cells stimulate B cells
  • w/ complimentary antibody on its surface
  • B plasma cells release large amounts of antibodies specific to antigen
  • B cells divide to form clones, all prod. same antibody
45
Q

describe the role of antibodies in prod. a +ve ELISA test

A
  • antibody binds to complimentary antigen
  • secondary antibody with enzyme is added
  • secondary antibody attaches to antigen
  • substrate added and color changes
46
Q

Describe how HIV replicates (10)

A
  1. The HIV’s attachment proteins binds to the CD4 receptor proteins on the surface of the Th cell.
  2. The virus’s lipid envelope fuses with the cell membrane of the Th cell.
  3. The protein capsid breaks down
  4. RNA and enzymes (e.g. reverse transcriptase) of the virus are now released into the cytoplasm of the
    host cell.
  5. Reverse transcriptase converts the viral RNA to DNA.
  6. The viral DNA is incorporated into the cell’s DNA.
  7. The viral DNA can now be transcribed into mRNA
  8. Viral mRNA passes through the nuclear pore and attaches to a ribosome
  9. Viral mRNA is translated into viral proteins that can be assembled into new HIV particles.
  10. HIV particles bud off the Th cell (so that the Th cell’s membrane forms the lipid envelope of the
    virus).
47
Q

phagocytosis is non..

A

non-specific response. any non-self cell that is detected will trigger the same response to destroy it.

48
Q

What is HIV?

A
  • When an HIV virus infects a TH cell and replicates, the cells are killed.
  • As HIV spreads through the body and more TH cells are killed, the immune system weakens.
  • The weak immune system makes the individual highly susceptible to infection by other pathogens. This is AIDs.
49
Q

Describe the steps involved in replication of HIV

A
  1. HIV attachment protein binds to comp. CD4 receptor proteins on surface of Th cell
  2. virus’ lipid envelope fuses w/ Th cell memb.
  3. RNA and reverse transcriptase released into host cell cytoplasm
  4. rev. tran. coverts RNA into vDNA
  5. vDNA inserted into cell’s DNA
  6. can now be transcribed into mRNA
  7. vmRNA passes through nuclear pore and attaches to ribosome
  8. -> translated into viral proteins -> assempled into HIV particles
  9. -> bud off the Th cell and infect another cell
50
Q

This person developed a large number of infections about 9 years after HIV infection. Explain why. (5)

A
  • more HIV produced leads to fall in T cells
  • HIV destroys T cells
  • so fewer T cells activate B cells / memory cells
  • reduced / no antibody production
  • immune system unable to fight infection
51
Q

H bonding requires:

A

H atom to be directly bonded to a N/O/F atom

52
Q

Explain how HIV affects production of antibodies when AIDS develop. (3)

A
  • less/no antibodies formed
  • HIV destroys T helper cells
  • fewer B cells activated
53
Q

With reference to the immune system, explain the importance of cell-cell recognition: (3)

A
  • to recognise pathogens so that T-helper and B lymphocytes can be activated
  • to recognise abnormal/cancerous cells so that they can be destroyed by T lymphocytes
  • ability to recognise self and non-self cells so non-self can be targeted by B lymphocytes/antibodies

only T cells can destroy self cells/abonormal self cells

54
Q

Explain why antibody A only attaches to protein found in the species of plasmodium. (2)

A
  • Antibody has tertiary structure.
  • complementary to binding site on protein.
55
Q

Suggest why Ranavirus is now able to infect different species of frogs even though before only one would get infected. (2)

A
  • mutation in viral DNA
  • altered (tertiary structure of) attachment proteins
56
Q

Determining the genome of the virus could allow the scientists to develop a vaccine. Explain how. (2)

A
  • could identify proteins that derive from the genetic code
  • to identify what antigen to use in the vaccine
57
Q

B plasma cells:

A

release complimentary AB to antigen

58
Q

A mother infected w/ HIV gave birth to a baby that tested positive for antibodies against HIV using ELISA test. Explain why this does not prove the baby is infected: (2)

A
  • children receive HIV anibodies from mother
  • so test will always be positive
59
Q

Explain how HIV leads to death (3)

A
  • susceptible to other pathogens
  • damage cells
  • release toxins
60
Q

When talking about AB and plasma cells:

A

plasma cells RELEASE antibodies

61
Q
A