Chapter 5 Cell recognition and immune system Flashcards

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1
Q

What are the two types of defence mechanisms.

A

Cell mediated response involving T lymphocytes
Humoral respoense involving B lymphocytes

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2
Q

What are self cells

A

The body’s own cells and molecules

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3
Q

What are non-self cells

A

Cells or molecules that are foreign

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4
Q

Why is it important that the immune system can tell the difference between self cells and non-self cells

A

to defend from foreign materials
not destroy the organism’s own tissues when defending itself

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5
Q

What is the problem with organ/tissue transplants in humans, how can we solve this?

A

The immune system recognises the transplant as non-self and begins to attack the transplanted tissue
SOLUTIONS:
tissue matching (e.g. from relatives)
immunosuppressant drugs

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6
Q

Describe how lymphocytes are able to identify cells as ‘self’ or ‘non-self’

A

lymphocytes have receptors that exactly fit those of the body’s own self cells
these lymphocytes are destroyed/suppressed
only ones that stay are the ones that fit foreign material (non-self)

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7
Q

What are the 4 things that the immune system can identify

A

pathogens
non-self material
toxins
Tumors

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8
Q

Describe the process of phagocytosis

A
  • the phagocyte is attracted to the pathogen and it moves towards the pathogen along a conc. gradient
  • the phagocyte has several receptors on its CSM that attach to chemicals on the surface of the pathogen
  • phagocyte then engulfs the pathogen forming a phagosome
  • lysosomes within the phagocyte migrate towards the phagosome
  • the lysosome release their lysozymes into the phagosome, where they hydrolyse the pathogen’s cell walls, destroying it
  • the soluble products from the breakdown of the pathogen are absorbed into the cytoplasm of the phagosome
  • other cell debris is moved out of the cell by exocytosis
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9
Q

Where can phagocytes be found

A

In the blood

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10
Q

Which cells do phagocytes activate

A

T-cells (they bind their own receptors to the complimentary antigens on the surface of phagocytes (antigen presentation))

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11
Q

What are antigens

A

Proteins that are located on the surface of cells which can trigger an immune response when detected by lymphocytes

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12
Q

What does the presence of antigens trigger

A

Presence of antigens triggers a production of antibodies or other specific immune response

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13
Q

What are the 2 types of lymphocytes and where do they develop

A

T cells: produced in bone marrow, mature in thymus gland
B cells: produced and matured in bone marrow

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14
Q

How can T lymphocytes distinguish invader cells from normal cells

A

phagocytes that have engulfed and hydrolysed a pathogen present some of a pathogen’s antigens on their own CSM
body cells invaded by a virus present some of the viral antigens on their own CSM
transplanted cells from individuals of the same species have different antigens on their CSM
Caner cells are different from normal body cells and present antigens on their CSM

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15
Q

What is cell-mediated immunity

A

When the T helper lymphocytes only respond to antigens that are presented on a body cell

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16
Q

What are the steps in a lymphocyte responding to an antigen

A
  1. Pathogens invade body cells or are taken in by phagocytes.
  2. The phagocyte places antigens from the pathogen on its cell- surface membrane.
  3. Receptors on a specific helper T cell (T cell) fit exactly onto these antigens.
  4. This attachment activates the T cell to divide rapidly by mitosis and form a clone of genetically identical cells.

5 The cloned T cells:

  • develop into memory cells that enable a rapid response to future infections by the same pathogen
  • stimulate phagocytes to engulf pathogens by phagocytosis
  • stimulate B cells to divide and secrete their antibody
  • activate cytotoxic T cells (Tc cells).
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17
Q

What do cytotoxic cells do

A

kill abnormal cells and any infected body cells
they produce a protein called perforin
it makes holes in CSM, compromising
the holes means = cell membrane becomes freely permeable to all substances and the cell dies as a result

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18
Q

Why is the action of T-helper cells most effective against viruses

A

because viruses use living cells in which to replicate
the sacrifice of body cells prevents viruses multiplying and infecting more

19
Q

Are antibodies soluble?

A

yes,
they’re soluble in the blood and tissue fluid of the body

20
Q

How many types of B cells are there

A

millions
each one producing a specific antibody that responds to a specific antigen
for every antigen on the surface of a pathogen, foreign cell, toxin, damaged or abnormal cell = there will be one B cell that has an antibody on its surface that is complementary to the antigen

21
Q

Describe the process of Humoral immunity

A

Antigen on surface of pathogen, foreign cell, toxin, damaged/abnormal cell enters the blood or tissue fluid
the antigen enters the B cell (with the complimentary antigen on its surface) by endocytosis and processes the them, then presents them on its surface
T-helper cells bind to these processed antigens and stimulate this B cell to divide by mitosis
forming clones of identical B cells, that produce the specific antibodies that work specifically for specific foreign antigens (clonal selection/expansion)
antibodies attaches to antigens on the pathogen and destroys them
Some B cells develop into memory cell. These can respond to future infections by the same pathogen by dividing rapidly into plasma cells

22
Q

What is the primary response in humoral immunity

A

plasma cells
secrete antibodies directly + then produce memory cells (in case infected again)
they only survive a few days
response is slow and person will get ill before pathogen is killed

23
Q

What is the secondary response in humoral immunity

A

memory cells
They circulate in blood + tissue fluid
when they encounter the antigen from the primary response they divide rapidly
response is rapid and person will not get ill

24
Q

What is the difference between Humoral and Cell-mediated immunity

A

HI = B lymphocytes, CMI = T lymphocytes
HI = produced and matured in bone marrow, CMI = produced in bone marrow, matures in thymus gland
HI = produces antibodies, CMI = doesn’t
HI = pathogens are identified by the antigens in the blood by binding to B cell receptors, CMI = pathogens are identified by the antigens on the surface of infected cells or phagocyte, a cancer cell or a transplant cell
HI = pathogens are killed when antibodies attach to antigens, CMI = cytotoxic cells
Hi = once stimulated, B cells divide into either plasma or memory cells, CMI = once stimulated, T cells divide by mitosis into specialist cells, e.g. T-helper cells or cytotoxic cells

25
Q

What are antibodies

A

proteins with specific binding sites synthesised by B cells

26
Q

Describe the structure of an antibody

A

made up of 4 polypeptide chains, the chains of one pair = long (called heavy chains), while the chain of the other pair = shorter (called light chains)
specific binding site for each antibody, fits precisely to the antigen to form: antigen-antibody complex
the different binding sites on each antibody is known as: variable region
each binding site consists of a sequence of amino acids that form the specific 3D shape that binds directly to a specific antigen
the rest of the antibody is known as the constant region, its the same for all antibodies. It binds to the receptors on cells such as B cells

27
Q

How does the antibody lead to the destruction of the antigen

A

antibodies don’t destroy antigens, but prepare the antigen for destruction in a different range of ways for each antibody:

1) agglutination - clumps of bacterial cells are formed, making it easier for the phagocytes to locate them (because they’re less spread-out within the body)
2) They then serve as markers that stimulate phagocytosis to engulf the bacterial cells to which they are attached

28
Q

Explain how a change in the primary structure of a globular protein may result in a different 3D structure, and the consequence of this on the immune response (5 marks)

A
  1. Primary structure is the sequence of amino acids
  2. Determines positioning of bonds and therefore tertiary structure
  3. This determines shape of variable region of antibody which is specific/complementary to one type of antigen
  4. change in the variable region = the antigen can no longer bind/no antigen-antibody complex formed
  5. Pathogen can no longer be formed
29
Q

How are monoclonal antibodies used in pregnancy testing

A

The placenta in a pregnant woman produces a hormone called hCG (human chorionic gonadotropin). This can be found in the mother’s urine.
Monoclonal antibodies are immobilised in coloured beads on a test strip.
When urine is applied, any hCG will bind to the antibodies to form antigen-antibody complexes.
The hCG-antibody-colour complex moves along the strip until it is trapped by a different type of antibody. The complexes accumulate to produce a coloured line (blue if hCG is present) to confirm pregnancy.

30
Q

What are the steps used in the ELISA test

A
  1. Apply the sample to a surface such as a slide
  2. Wash the surface several times to remove any unattached antigens
  3. Add the antibody that is specific to the antigen we are trying to test for and leave the two to bind
  4. Wash the surface to remove excess antibody
  5. Add a second antibody that binds to the first antibody. The second antibody has an enzyme attached to it.
  6. Wash the surface again.
  7. Add the colourless substrate of the enzyme. The enzyme acts on the substrate to change it into a coloured product.

The amount of antigen represent is relative to the intensity of the colour produced.

31
Q

What are the 2 types of immunity

A

Active immunity
Passive immunity
—> both can be artificial or natural

32
Q

What is passive immunity + example

A
  • produced by the introduction of antibodies into individuals from an outside source
  • No direct contact with the pathogen or its antigen is necessary to induce immunity
  • immunity is acquired immediately
  • As the antibodies aren’t being produced by the individual = they cannot be replaced when they’re broken down because no memory cells are produced. Hence why passive immunity gives no long lasting immunity
  • NATURAL PASSIVE IMMUNITY EXAMPLE: Antibodies received from mother via breast milk or placenta
  • ARTIFICIAL PASSIVE IMMUNITY EXAMPLE: injection of antiserum containing antibodies, e.g. anti-venom
33
Q

What is Active immunity + examples

A
  • is produced by stimulating the production of antibodies by the individuals’ own immune system.
  • Direct contact with the pathogen or its antigen is necessary
  • immunity takes time to develop, but is long-lasting
  • NATURAL ACTIVE IMMUNITY EXAMPLE: Being infected and recovering from a pathogen
  • ARTIFICIAL ACTIVE IMMUNITY EXAMPLE: vaccination = antigens are received in a jab
34
Q

Describe how vaccines work (5 marks)

A

Vaccines contain antigens and are injected
Body fights dead pathogens/weakened pathogens
Memory cells are made
On 2nd exposure memory cells produce antibodies/become active
Rapidly producing antibodies in high quantities, lasting longer
Antibodies destroy pathogens
Leads to herd effect as fewer people pass on the disease

35
Q

What is the key things to remember about a secondary response

A

antibodies are created quicker
antibodies are created in higher quantities
last longer

36
Q

What is herd immunity

A

It arises when a sufficiently large proportion of the population has been vaccinated to make it difficult for a pathogen to spread within that population

37
Q

How is HIV transmitted

A

HIV is a retrovirus
not transmitted by a vector
HIV is unable to survive outside the human body
the virus is spread by intimate human contact and can only be transmitted by direct exchange of body fluids

38
Q
A
  • Following infection, HIV enters the bloodstream and circulates around the body
  • A protein on the HIV readily bonds to a protein called CD4. While this protein occurs on a number of different cells. HIV most frequently attaches to T-helper cells
  • the protein capsid fuses with the CSM. The RNA and enzymes of HIV enter the T-helper cells
  • The HIV reverse transcriptase converts the virus’s RNA into DNA
  • the newly made DNA is moved into the T-helper cell’s nucleus where it is inserted into the cell’s DNA
  • the HIV DNA in the nucleus creates mRNA using the cell’s enzymes. This mRNA contains the instructions for making new viral proteins and the RNA to go into the new HIV
  • the mRNA passes out of the nucleus through a nuclear pore and uses the cell’s protein synthesis mechanisms to make HIV particles
  • The HIV particles break away from the T-helper cells with a piece of its CSM surrounding them which forms their lipid envelope
39
Q

What are the key components of HIV

A

2 RNA strands
proteins (including reverse transcriptase)
a protein coat (capsid)
A viral envelope consisting of a lipid bilayer and glycoproteins (the lipid bilayer is derived from the cell membrane of host t-helper cells that the particle escaped from
attachment proteins

40
Q

How does HIV cause the symptoms of AIDS

A

causes AIDS by killing/interfering with the normal functioning of T-helper cells
T helper cells :
1) stimulate B cells to produce antibodies
2) stimulate cytotoxic T cells that destroys cells infected by pathogens
3) memory cells may also become infected and destroyed

41
Q

Describe what antibiotics do to bacteria

A

Antibiotics like penicillin inhibits certain enzymes required for synthesis and assembly of the peptide cross-linkages in bacterial cell walls
This weakens the walls, making them unable to withstand pressure
as water enters naturally by osmosis, the cell bursts and the bacterium dies

42
Q
A
43
Q

Why does a mutation cause the immune system to no longer work against that pathogen

A

A mutation can cause a change in the primary structure of a protein leading to a change in its tertiary structure and an alteration to the shape of the antigen.

The immune system will only be effective against the unmutated pathogen as all of the memory cells have the old antigen shape

This is known as antigen variability