immunology Flashcards

1
Q

state 2 ways that pathogens cause harm/disease?

A
  • pathogen can produce toxins which can directly damage tissue
  • pathogen can sometimes replicate inside and destroy host cells
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2
Q

def: antigen

A

a molecule (protein),
which can be recognised as non self by immune system,
stimulates an immune response,
and leads to the production of a specific antibody

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3
Q

def: phagocytes

A

group of white blood cells, can distinguish between cells with or without self antigen

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4
Q

non-specific immune system:

A

1.phagocyte recognises foreign antigens on the pathogen and binds to the antigen
2. pathogen is engulfed by the phagocyte
3. engulfed pathogen enters the cytoplasm of the phagocyte in a vesicle
4. lysosomes fuse with the vesicle releasing lysozymes (hydrolytic enzymes)
5. lyzozymes hydrolyse/digest the pathogen
6. waste materials are removed from the cell by exocytosis
7. phagocyte becomes an antigen presenting cell

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5
Q

limitation of non- specific immune response:

A

takes far too long to destroy the pathogens in an infection,
damage tissue + organs

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6
Q

specific immunity:

A

a specific response to a specific antigen on the surface of a cell or pathogen that has been recognised as non-self

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7
Q

what is an antibody?

A

a globular quaternary protein,
made in response to a specific antigen,
produced by B cells
and secreted by plasma cells

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8
Q

where are antigens found and what are their use?

A

on the cell surface membranes, which are identified as self and non self via these specific antigens

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9
Q

name 4 types of foreign antigens

A

Pathogens - organisms causing disease
Abnormal body cells - cancerous/infected cells
Toxins - poisonous molecules
Cells from other organisms - transplant cells

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10
Q

why is phagocytosis part of non-specific immunity?

A

works the same for any foreign antigen

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11
Q

what are phagocytes?

A

white blood cells which ingest/engulf and destroy any cells presenting a non-self-antigen.

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12
Q

what are the cons of phagocytosis?

A

takes too long and can result in damage to tissues, organs

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13
Q

explain phagocytosis

A

1.Pathogen engulfed by phagocyte
2.Pathogen enters the cytoplasm in a vesicle called phagosome
3.Lysosome fuses with phagosome releasing lysozymes (hydrolytic digestive enzymes)
4.Lysozymes hydrolyse the pathogen and waste materials are released via exocytosis
5.Antigens are presented on the cell membrane making the phagocyte an antigen presenting cell

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14
Q

def: specific immunity

A

responds to a specific antigen on the surface of a cell/ phagocyte which has been recognised as non self

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15
Q

what are T-cells

A

white blood cells with specific receptor proteins on the surface which bind to specific antigens on antigen presenting cells

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16
Q

what is the cell mediated
response

A

involves t-cells

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17
Q

what are TH cells (T helper cells)

A

respond directly to pathogen/antigen or the antigen presenting cells

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18
Q

describe the process of T cell clonal selection

A

1.T helper cell with specific complementary receptor protein binds to antigen on antigen presenting cell becoming activated
2. This then rapidly divides via mitosis producing more T helper cells
3.These clone cells are then differentiated into 3 different types

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19
Q

Describe the 3 types of T cells

A

TH - Specific receptor protein binds to specific antigens releasing cytokines which attracts phagocytes to the area, stimulates specific B cells and activates Tc cells.
T memory cells - remain in the blood in case of re infection
Cytotoxic T killer cells Tc - Locates and destroys virally infected and cancer cells. Binds to antigens and releases perforin which create holes in the cell membrane destroying the cells

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20
Q

Why is clonal selection of T cells needed

A

Not enough room in body for lots of T cells to be stored, and would increase total energy demands of organism so instead are cloned on demand

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21
Q

Explain the humoral response

A

1.Specifc THcell releases cytokines when bound to specific antigen stimulating specific B cell
2.Specific B cell undergoes rapid mitosis producing clones
3.These then differentiate into B plasma and B memory cells

22
Q

Explain the function of B plasma cells

A

Produce and secrete large amounts of specific antibodies into the blood plasma

23
Q

Explain the function of B memory cells

A

Remain in blood stream to rapidly respond to pathogens if re-infection occurs.
They are rapidly activated by cytokines and more quickly cloned by mitosis into plasma cells and more b cells
These plasma cells then produce higher concentrations of antibodies at a quicker rate

24
Q

What is the secondary response

A

Activation of memory cells to produce antibodies more quickly and in higher
concentrations, eliminating the antigen before symptoms develop

25
Q

Draw and label the structure of an antibody

A

Globular quaternary protein made of 4 polypeptide chains
Main part is a constant region. The variable regions have a different primary structure therefore a different tertiary structure making the binding sites for antigens specific and complementary. This allows antigen antibody complexes to form
Disulphide bridges in the base of heavy chain, variable region is light.

26
Q

Describe 2 ways in which antibodies aid immune
response

A

Agglutination - Each antibody has 2 binding sites. Specific antibodies bind to specific antigens on pathogens clumping them together. This attracts phagocytes to destroy many pathogens at once
Opsonisation - Antibodies mark pathogens so phagocytes can recognise and destroy pathogens more efficiently

27
Q

Explain how lysis and antitoxins/antivenom aid the immune svstem

A

Lysis - antibody binds to antigen and destroys pathogen membrane
Anti-venom - Binds to venom/ toxins and causes its destruction.
May also prevent their replication and prevent them binding to target receptors

28
Q

Compare the primary and secondary response

A

Primary exposed to antigen for first time, not many t or b cells. Symptoms of disease shown, antibodies slowly produced and t memory cells.
Secondary clonal selection occUrs faster from t memory cells and b cells and more antibodies are more rapidly produced, no symptoms show.

29
Q

When is the secondary response effective

A

If pathogens have the same antigens on their surface as they can be recognised by b memory cells

30
Q

Explain antigenic variability

A

Antigens on the surface of pathogens can mutate. This means primary structure is different, resulting in a different tertiary structure which means the antigen has a different shape. It will not be recognised by the b memory cells and it is no longer complementary to the receptor proteins

31
Q

How can vaccines be developed to overcome antigenic variability

A

Use all of the different strains of a pathogen to produce a range of different antibodies to the different mutated antigens

32
Q

Explain the differences between active and passive immunity

A

Passive - no antigen exposure, no memory cells produced, short term protection as antibodies get broken down, immediate protection, antibodies received from elsewhere e.g.
breast milk/placenta

33
Q

Explain how vaccines are made

A

1.Dead/weakened antigen from pathogen injected into body and macrophage presents antigen on its cell membrane
2.T-cells with complementary receptor protein binds to antigen releasing cytokines
3.This stimulates specific b cell to rapidlv divide by mitosis
4.This produces plasma b cells which secrete antibodies in large numbers and memory b cells which remain in blood 5.1f antigens present again, plasma cells more rapidly produced and produce more antibodies quicker and in higher concentrations

34
Q

What is herd immunity

A

If majority (85%+) population vaccinated there is little chance for disease to spread even to non-vaccinated as less people to pass it on

35
Q

What are 3 side effects to vaccines

A

1.Complications/unexpected health problems
2.If taken orally enzymes may break down in gut, or molecules may be too large to be absorbed into blood
3.Boosters needed to ensure more memory cells are produced

36
Q

Give 5 ethical issues to vaccines

A

1.Must be tested on animals first
2.Must also be tested on humans
3.Economic/affordability issues
4.Risks vs effectiveness
5.Herd immunity - unfair

37
Q

What are monoclonal antibodies

A

Antibodies with same tertiary structure cloned from the same plasma cell which bind specifically to one antigen

38
Q

What are 5 uses of monoclonal antibodies

A

1.Research
2.Immunoassays
3.Diagnosis
4.Targeting drugs to specific cell types
5.Killing specific cells

39
Q

What is an ethical issue to monoclonal antibodies

A

Involves tumour cells in mice and human volunteers with unexpected side effects

40
Q

What is the Elisa test used for

A

To test if a patient has
antibodies to a certain antigen or vice versa, and to test for pathogenic infections

41
Q

Explain the direct Elisa test

A

1.Antigens bound to inside of the well
2.complementory antibody to antigen added
3. 2nd antibody with enzyme attached added
4. Washed to remove unbound antibodies
5.substrate solution added which changes colour if antigen present

42
Q

Explain how the Elisa test is used for HIV

A

1.HIV antibodies bound to bottom of testing well
2.Blood sample containing many antigens added
3. Any specific antigens bind to antibodies becoming immobilised
4.Wash solution and add second antibody with enzyme attached
5.Binds to any complementary antigens
6.wash so any unbound enzyme antibodies washed away
7.Add substrate solution, colour change indicates HIV positive

43
Q

Describe the structure of HIV

A

Lipid viral envelope (X2) , attachment proteins, Reverse transcriptase and RNA inside the capsid

44
Q

What does HIV do

A

Effects the immune system by infecting and killing T helper cells compromising cell mediated immunity

45
Q

Explain the process of HIV replication

A

1.Attachment protein on HIV binds to receptor molecule on
TH cell
2.Capsid fuses with cell membrane and is released into the cell, uncoating and releasing Viral RNA and enzymes
3.Reverse transcriptase makes complementary DNA from
RNA template using host nucleotides which is then made double stranded
4. The viral cDNA moves into TH cell nucleus and is inserted into host cell’s DNA. Person is now infected
5.The viral DNA is then transcribed into viral mRNA to produce HIV proteins… 6.These proteins are assembled into new
HIV viruses and break away from T cell which forms the lipid envelope with TH receptors embedded.
7.The t cell then ruptures and dies

46
Q

Give 5 ethical issues to vaccines

A

1.Must be tested on animals first
2.Must also be tested on humans
3.Economic/affordability issues
4.Risks vs effectiveness
5.Herd immunity - unfair

47
Q

What are 3 side effects to vaccines

A

1.Complications/unexpected health problems
2.If taken orally enzymes may break down in gut, or molecules may be too large to be absorbed into blood
3.Boosters needed to ensure more memory cells are produced

48
Q

Describe how AIDS develops

A

1.A high viral load leads to large destruction of TH cells
2.There is less activation of B cells and T cells
3.Less plasma cells and antibodies produced
4.Less able to destroy other pathogens/ mutate cells/cancer cells
5.Secondary infections develop

49
Q

Give 2 ways aids is diagnosed

A

1.Symptoms of secondary infections
2.Lack of T helper cells

50
Q

Why can aids not be detected by antibodies

A

not a pathogen

51
Q

How do antibiotics attack bacteria

A

Prevent bacterial cell wall forming by attacking 70s ribosomes
No cell wall means unable to resist osmotic pressure, cell bursts due to too much water entering via osmosis.

52
Q

Why are antibiotics not effective against viruses

A

Viruses have no organelles to disrupt as they use host cell to replicate and carry out metabolic activity. They also have a capsid instead of cell wall and spend most time in host cell so hard to target.