2.4 Cell Recognition & the Immune System Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

What is an antigen?

A

Cell surface molecule which stimulate immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does the immune system recognise antigens?

A

As “self” or “non-self”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is antigen recognition useful for?

A

Enables identification of cells from other organisms, pathogens, toxins and abnormal body cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe how phagocytosis destroy pathogens.

A
  1. Phagocyte moves towards pathogen via chemotaxis
  2. Phagocyte engulfs pathogen via endocytosis to form a phagosome
  3. Phagosome fuses with lysosome to form phagolysosome
  4. Lysozymes digest pathogen
  5. Phagocyte absorbs the products from pathogen hydrolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does APCs stand for?

A

Antigen-Presenting Cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is an antigen-presenting cell?

A

Macrophage displays antigen from pathogen on its surface after hydrolysis in phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why are APCs necessary?

A

Enhances recognition by helper T cells which cannot directly interface with pathogens/antigens in bidy fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Give two differences between specific and nonspecific immune responses.

A

Nonspecific is immediate - specific has a time lag
Nonspecific is the same for all pathogens - specific is complementary to pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Name the two types of specific immune response.

A

Cell mediated
Humoral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the process of cell-mediated response.

A
  1. Complementary helper T lymphocytes bind to foreign antigen on APC
  2. Release cytokines that stimulate:
    a) clonal expansion of complementary helper T cells - become memory cells ir trigger humoral response
    b) clonal expansion if cytotoxic T cells - secrete enzyme perforin to destroy infected cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the process of the humoral response.

A
  1. Complementary helper T lymphocytes bind to foreign antigen in antigen presenting T cells
  2. Release cytokines that stimulate clonal expansion of complementary B lymphocytes
  3. B cells differentiate into plasma cells
  4. Plasma cells secrete antibodies with complementary variable region to antigen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is an antibody?

A

Proteins secreted by plasma cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the quarternary structure of an antibody.

A

2 “light chains” held by disulfide bridges and 2 longer “heavy chains”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the regions of an antibody.

A

Binding sites on variable region of light chains have specific tertiary structure complementary to an antigen
The rest of the molecule is known as the constant region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do antibodies lead to the destruction of a pathogen?

A

Formation if antigen-antibody complex results in aggultination which enhances phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are monoclonal antibodies?

A

Antibodies produced from a single clone of B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are memory cells?

A

Specialised helper T cells or B cells produced from primary immune response
Remain in low levels in the blood

18
Q

What do memory cells do if organism encounters same pathogen again?

A

Divide rapidly by mitosis

19
Q

What are the advantages of the secondary immune response?

A

Faster rate of antibody production
Shorter time lag between exposure and antibody production
Higher concentration of antibodies
Antibody level remains higher after
Pathogen usually destroyed before symptoms

20
Q

What causes antigen variability?

A
  1. Random genetic mutation changes DNA base sequence
  2. Different sequence of codons on mRNA
  3. Different primary structure of antigen means different disulfide bridges and H and ionic bonding in tertiary structure
  4. Different shape of antigen
21
Q

Explain how antigen variability affects the incidence of disease.

A

Memory cells no longer complementary to antigen which prevents immunity so disease can be caught more than once
Many varieties of a pathogen makes a vaccine difficult to develop

22
Q

Describe similarities between passive and active immunity.

A

Both involve antibodies
Can both be natural or artificial

23
Q

Give an example of natural passive immunity.

A

Antibodies in breast milk/placenta

24
Q

Give an example of artificial passive immunity.

A

Anti-venom

25
Q

Give an example of natural active immunity.

A

Humoral response

26
Q

Give an example of artificial active immunity.

A

Vaccination

27
Q

Describe differences between passive and active immunity.

A

Active long term - passive short term
Active time lag - passive immediate
Active lymphocytes produce antibodies - passive antibodies from external source
Active requires direct contact with antigen - passive doesnt require direct contact with antigen

28
Q

Why is active immunity long term?

A

Memory cells produced

29
Q

Why is passive immunity short term?

A

No memory cells are produced
Antibodies are not replaced when broken down

30
Q

Describe how vaccinations function.

A
  1. Vaccine contains dead/inactive form of a pathogen or antigen
  2. Triggers primary immune response
  3. Memory cells produced and remain in bloodstream
  4. Pathogen is destroyed before symptoms
  5. Upon reinfection, secondary response is rapid and produces higher concentration of antibodies
31
Q

What is herd immunity?

A

Vaccinating large proportion of the population reduces available carriers of the pathogen so protects those who are unvaccinated

32
Q

Suggest ethical issues surrounding vaccine use.

A

Production may involve animals
Potentially dangerous side effects
Clinical tests may be fatal

33
Q

Describe the structure of HIV.

A

RNA and viral enzymes surrounded by capsid
Surrounded by viral envelope derived from host cell membrane
GP120 attachment proteins on surface

34
Q

How does HIV result in the symptoms of AIDS?

A
  1. Attachment proteins bind to complementary receptor on helper T cells
  2. HIV virus replicates inside helper T cells, killing or damaging them
  3. AIDS develops when there are too few helper T cells for the immune system to function
  4. Individuals cannot destroy other pathogens and suffer from secondary diseases
35
Q

Why are antibiotics ineffective against viruses?

A

Antibiotics often work by damaging murein cell walls to cause osmotic lysis - viruses have no cell walls

36
Q

Why are viruses difficult to destroy?

A

Viruses replicate inside host cells so it is difficult to destroy them without damaging normal body cells

37
Q

Suggest the clinical applications of monoclonal antibodies.

A

Pregnancy tests - detection of HCG hormones in urine
Diagnostic procedures e.g. ELISA test
Targeted treatment by attaching drug to antibody

38
Q

Explain the principle of a direct ELISA test.

A

To detect the presence of a specific antigen

39
Q

Explain how a direct ELISA test works.

A
  1. Monoclinal antibodies bind to bottom of test plate
  2. Antigen molecules in sample bind to antibody and rinse excess
  3. Mobile antibody with enzyme attached binds to antigens that are fixed on the monoclonal antibodies and rinse excess
  4. Add substrate for enzyme - positive result is colour change
40
Q

Explain the principle of an indiret ELISA test.

A

To detect presence of an antibody against a specific antigen

41
Q

Explain how a indirect ELISA test works.

A
  1. Antigens bind to bottom of test plate
  2. Antibodies in sample bind to antigen and rinse excess
  3. Secondary antibody with enzyme attached binds to primary antibodies from the sample
  4. Add substrate for enzyme - positive result is colour change
42
Q
A