2.4 Cell Recognition And The Immune System Flashcards

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1
Q

What is an antigen?

A
  • Cell surface membrane which stimulate immune response
  • Usually glycoprotein, sometimes glycolipid or polysaccharide
  • Immune system recognises as ‘self’ or ‘non-self’ = enables identification of cells from other organisms of same species, pathogens, toxins and abnormal body cells
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2
Q

How does phagocytosis destroy pathogens?

A
  1. Phagocyte moves toward pathogen via chemotaxis
  2. Phagocyte engulfs pathogen via endocytosis
  3. Phagosome fuses with lysosome
  4. Lysozymes digest pathogens
  5. Phagocyte absorbs the 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
  • Enhances recognition of helper T 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 - same for all pathogens, specific - complementary pathogen
  • Nonspecific - immediate, specific - time lag
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5
Q

Name two types of specific immune response

A
  • Cell mediated
  • Humoral
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6
Q

Outline the process of the cell-mediated response

A
  1. Complementary helper T lymphocytes bind to foreign antigen on APC
  2. Release cytokines that stimulate clonal expansion of complementary helper T cells and clonal expansion of cytotoxic T cells
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7
Q

What is clonal expansion of complementary helper T cells?

A

Become memory cells or trigger humoral response

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8
Q

What is clonal expansion of cytotoxic T cells?

A

Secrete the enzyme perforin to destroy infected cells

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9
Q

Outline the process of the humoral response

A
  1. Complementary T helper lymphocytes bind to foreign antigen on 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
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10
Q

What is an antibody?

A
  • Proteins secreted by plasma cells
  • Quaternary structure: 2 ‘light chains’ held together by disulfide bridges, 2 longer ‘heavy chains’
  • Binding sites on variable region of light chains have specific tertiary structure complementary to an antigen
  • The rest of the molecule is known as a constant region
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11
Q

How do antigens lead to the destruction of a pathogen?

A

Formation of antigen-antibody complex results in agglutination, which enhances phagocytosis

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12
Q

What are monoclonal antibodies?

A

Antibodies produced from a single clone of B cells

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13
Q

What are memory cells?

A
  • Specialised T helper cells/ B cells produced from primary immune response
  • Remain in low levels in the blood
  • Can divide very rapidly by mitosis if organism encounters the same pathogen again
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14
Q

Contrast the primary and 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 the secondary response
  • Pathogen usually destroyed before any symptoms
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15
Q

What causes antigen variability?

A
  • Random genetic mutation changes in DNA base sequence
  • Results in different sequence of codons on mRNA
  • Different primary structure of antigen = H bonds, ionic bonds and disulfide bridges form in different places in the tertiary structure
  • Different shape of antigen
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16
Q

Explain how antigen variability affects the incidence of disease

A
  • Memory cells no longer complementary to antigen = individual not immune = can catch the disease more than once
  • Many varieties of a pathogen = difficult to develop vaccine containing all antigen types
17
Q

Compare passive and active immunity

A
  • Both involve antibodies
  • Can be both natural or artificial
18
Q

Examples of passive natural immunity

A

Antibodies in breast milk/across placenta

19
Q

Examples of passive artificial immunity

A

Anti-venom, needle stick injections

20
Q

Examples of active natural immunity

A

Humoral response to infection

21
Q

Examples of active artificial immunity

A

Vaccination

22
Q

Contrast passive and active immunity

A
  • Passive: no memory cells and antibodies not replaced when broken down = short term, active: memory cells produced = long term
  • Passive: immediate, active: time lag
  • Passive: antibodies from external source, active: lymphocyte produce antibodies
  • Passive: direct contact with antigen not necessary, active: direct contact with antigen necessary
23
Q

Explain the principles of vaccination

A
  1. Vaccine contains dead/inactive form of a pathogen or antigen
  2. Triggers primary immune response
  3. Memory cells are produced and remain in the bloodstream, so secondary response is rapid and produces higher concentration of antibodies
  4. Pathogen is destroyed before it causes symptoms
24
Q

What is herd immunity?

A
  • Vaccinating a large proportion of population reduces available carriers of the pathogen
  • Protects individuals who have not been vaccinated e.g. those with a weak immune system
25
Q

Suggest some ethical issues surrounding the use of vaccine

A
  • Production may involve use of animals
  • Potentially dangerous side effects
  • Clinical tests may be fatal
  • Compulsory vs opt out
26
Q

Describe the structure of HIV

A
  • Genetic material (2x RNA) and viral enzymes surrounded by capsid
  • Surrounded by viral envelope derived from host cell membrane
  • GP120 attachment proteins on surface
27
Q

How does HIV result in symptoms of AIDs?

A
  1. Attachment proteins bind to complementary CD4 receptor on T helper cells
  2. HIV particles replicate inside T helper cells, killing or damaging them
  3. AIDS develops when there are too few T helper cells for the immune system to function
  4. Individuals cannot destroy other pathogens and suffer from secondary diseases/infections
28
Q

Why are antibiotics ineffective against viruses?

A
  • Antibiotics often work by damaging murein cell walls to cause osmotic lysis
  • Viruses have no cell wall
  • Viruses replicate inside host cells = difficult to destroy them without damaging normal body cells
29
Q

Suggest the clinical applications of monoclonal antibodies

A
  • Pregnancy tests by detecting HCG hormones in urine
  • Diagnostic procedures e.g. ELISA test
  • Targeted treatment by attaching drug to antibody so that it only binds to cells with abnormal antigen
30
Q

Explain the principle of the direct ELISA test

A
  1. Monoclonal antibodies bind to the bottom of the test plate
  2. Antigen molecules in the sample bind to the antibody. Rinse excess
  3. Mobile antibody with ‘reporter enzyme’ attached binds to antigens that are ‘fixed’ on the monoclonal antibodies. Rinse excess
  4. Add substrate for reporter enzyme. Positive result: colour change
31
Q

What does a direct ELISA test do?

A

Detect the presence of a specific antigen

32
Q

Explain the principle of an indirect ELISA test

A
  1. Antigens bind to the bottom of the test plate
  2. Antibodies in sample bind to antigen. Wash away excess
  3. Secondary antibody with ‘reporter enzyme’ attached binds to primary antibodies from the sample
  4. Add substrate for reporter enzyme. Positive result: colour change
33
Q

What does an indirect ELISA test do?

A

Detects the presence of an antibody against a specific antigen

34
Q

Suggest some ethical issues surrounding the use of monoclonal antibodies

A
  • Production involves animales
  • Drug trials against arthritis and leukaemia resulted in multiple organ failures