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Immunology Flashcards

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1
Q

State 2 ways that pathogens can cause harm/disease (2)

A

Produce toxins which can directly damage tissues
Can sometimes replicate inside and destroy host cells

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2
Q

What is an antigen? (1)

A

A foreign protein that stimulates an immune response that results in the production of a specific antibody

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3
Q

What is a phagocyte? (1)

A

White blood cell that engulf and destroy any cell that presents a non-self-antigen

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4
Q

Describe the process of phagocytosis (4)

A

Pathogen engulfed by phagocyte (endocytosis) into the cytoplasm and in a vesicle which is called a phagosome
Lysosomes fuse with phagosome releasing hydrolytic enzymes which hydrolyses the pathogen
Waste materials released from the cell by exocytosis
Antigens presented on the cell surface membrane and the phagocyte becomes an antigen presenting cell

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5
Q

Give 2 differences between specific and non-specific immune responses
Name the two types of specific immunity (4)

A

Non-specific: (phagocytosis) same for all pathogens
Specific: (B and T lymphocytes)
Non-specific: immediate
Specific: time lag
Cell mediated and humoral response

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6
Q

Outline the process of the cell mediated response (4)

A

T helper cell with specific receptors binds to complementary antigen on APC
Cytokines released which:
Stimulate clonal expansion of complementary T helper cells - become memory cells or trigger humoral response
Stimulates clonal expansion of cytotoxic T cells- secrete enzyme perforin to destroy infected cells

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7
Q

Role of Cytotoxic killer T cells (2)

A

Locate and destroy infected body cells that present the correct antigen
Bind to APC (antigen-presenting-cells)

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8
Q

Outline the process of the humoral response (4)

A

Specific T helper cell with specific receptor binds to complementary antigen and activates a specifically complementary B cell
Cytokines (released by specific T helper cell) signal the specific B cell to clone by mitosis
B cells differentiate into plasma cells and memory (B) cells
Plasma cells secrete antibodies

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9
Q

What is the role of memory (B) cells? (1)

A

Remain in the body to respond to pathogen rapidly and extensively if there is a future re-infection

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10
Q

Contrast the primary and secondary immune response (9)

A

Primary:
Initial response when a pathogen is encountered
Small number of antibodies
Slower rate of antibody production
Secondary:
Re-exposure to same antigen
Faster rate of antibody production
Higher concentration of antibodies
Antibodies level remain higher after the secondary response
Shorter time lag between exposure and antibody production
Pathogen usually destroyed before any symptoms

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11
Q

What causes antigen variability? (4)

A

Random genetic mutation changes DNA base sequence
Results in different sequence of codons on mRNA
Different primary structure of antigen = H-bonds, ionic bonds and disulphide bridges form in different places in tertiary structure
Different shape of antigen

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12
Q

Explain how antigen variability affects the incidence of disease? (2)

A

Memory cells no longer complementary to antigen - individual no immune - can catch the disease more than once
Many varieties of a pathogen - difficult to develop vaccines containing all antigen types

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13
Q

What is an antibody? (2)

A

A protein made in response to a foreign antigen which has a binding site which binds specifically to an antigen.
Produced by specific plasma cells

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14
Q

Describe the structure of an antibody (4)

A

Quaternary structure - 4 polypeptide chains
2 light chains bonded to 2 longer heavy chains
Constant region: main part of antibody which is the same in all antibodies
Variable region: different primary structure so different tertiary structure
Disulphide bridge - joins two different polypeptides

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15
Q

How do antibodies destroy pathogens? (5)

A

Agglutination: specific antibodies bind to the antigen on pathogen and clump them together so that phagocytes can ingest them more easily
Opsonisation: marking pathogens so phagocytes recognise and destroy the pathogen more efficiently
Lysis: bind to antigens and lead to destruction of the pathogens membrane
Anti-toxin and anti-venom: bind to toxins or venom to prevent these molecules from binding to complementary target receptors
Prevent pathogen replication

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16
Q

What is passive immunity? (3)

A

The short-term immunity that results from the introduction of antibodies from external sources
No production of memory cells
No exposure to antigen

17
Q

What is active immunity? (3)

A

Antibodies produced in response to exposure to an antigen.
Provided by the memory cells that are produced after a primary immune response to a pathogen
Exposure to antigen

18
Q

Why are antibodies ineffective against viruses? (2)

A

Antibodies often work by damaging murein cell walls to cause osmotic lysis - viruses have no cell walls
Viruses replicate inside host cells - difficult to destroy them without damaging host cells

19
Q

How do vaccinations work? (7)

A

Vaccine contains antigen from pathogen
Macrophage presents antigen on its surface
T cell with complementary receptor protein binds to antigen
T cell stimulates B cell
(With) complementary antibody on its surface
B cell secretes large amounts of antibody;
B cell divides to form clone all secreting / producing same antibody.

20
Q

What kind of pathogens are vaccines ineffective against? (1)

A

Pathogens that show antigenic variability

21
Q

Why are booster vaccines sometimes administered? (2)

A

To make sure that memory cells are still present in the blood which increases efficiency of the vaccine
When the vaccine does not induce a strong response these can be given to maintain immunity

22
Q

How do vaccines provide herd immunity? (2)

A

When significant proportion of population is vaccinated, the pathogen is less likely to affect a non-immunised individual
Reduces available carriers of the pathogen

23
Q

What are the ethical issues with vaccinations? (4)

A

Development and testing involve use of animals - which can infringe rights of animals
Can cause potentially dangerous side effects
Vaccine is only available to those who can afford it (people in poor countries cannot)
Human testing - putting people at risk and it is mostly the poor people who choose to take part in trials

24
Q

What are monoclonal antibodies? (1)

A

Antibodies with the same tertiary structure made from identical/cloned B cells

25
Q

Uses of monoclonal antibodies (5)

A

Immuno assays (pregnancy tests and ELISA)
Diagnosis of disease
Research
Targeting drugs to specific cells/antigens
Killing specific cells

26
Q

How does the direct ELISA work? (7)

A

Detects presence of a specific antigen
Antibodies fixed to the surface of the test wall
Sample (blood or urine) containing the antigen binds to the antibody to form an antibody-antigen complex
Unbound antigens washed away
Antibodies with enzymes attached added and they bind to the antibody-antigen complex
Unbound antibodies with enzymes washed away
Substrate added which causes a colour change

27
Q

What is HIV? (2)

A

Human Immunodeficiency Virus which causes the disease Acquired Immune Deficiency Syndrome (AIDS)

28
Q

Outline how HIV replicates (6)

A

Attachment proteins on HIV bind with receptor proteins on T helper cells
HIV capsid fuses with the cell-surface membrane and releases the viral RNA and enzymes into the T helper cell
HIV’s reverse transcriptase converts the viral RNA to cDNA (complementary DNA) using the hosts nucleotides
The new DNA (viral cDNA) enters nucleus of the T cell and is inserted into host cell genome - person is now infected
Transcription of viral DNA into viral mRNA which is translated to produce HIV proteins.
Infected T helper cell produces new HIV particles which break away and take a section of the host cell surface membrane forming their lipid envelope with T helper receptor proteins embedded

29
Q

How does HIV reduce an individual’s ability to respond to pathogens? (2)

A

Compromises cell mediated immunity as it uses the body’s T helper cells to replicate
Over time it leads to a reduction in the number of T helper cells

30
Q

How can HIV be detected in a patient? (1)

A

By using the ELISA

31
Q

Why can AIDS not be detected by ELISA? (1)

A

AIDS is not a pathogen so cannot be detected using antigens or antibodies

32
Q

How can AIDS be detected? (2)

A

By checking the number of T helper cells
Symptoms

33
Q

How does the indirect ELISA work? (7)

A

Detects presence of a specific antibody against a specific pathogen
Antigens fixed to the surface of the test wall
Sample (blood or urine) containing the antibody binds to the antigen to form an antibody-antigen complex
Unbound antibodies washed away
Antibodies with enzymes attached added and they bind to the antibody-antigen complex
Unbound antibodies with enzymes washed away
Substrate added which causes a colour change

34
Q

Describe the difference between active and passive immunity (4)

A

Active involves memory cells whereas passive does not
Active involves production of antibody by plasma cells
Whereas passive involves antibody introduced into body from outside sources
Active is long term because antibody is produced in response to an antigen
Whereas passive is short term because antibody is broken down
Active can take time to develop/work whereas passive is fast acting

35
Q

How does HIV cause the symptoms of AIDS (3)

A

HIV infects and destroys T helper cells
Reduction in number of T helper cells reduces the immune response
Leaves people vulnerable to secondary diseases

36
Q

Describe the structure of HIV (5)

A

RNA (as genetic material)
Reverse transcriptase
(Protein) capsid
Phospholipid viral envelope
Attachment proteins

37
Q

Suggest some ethical issues surrounding the use of monoclonal antibodies (1)

A

Production involves animals

38
Q

Tests using monoclonal antibodies are specific. Use your knowledge of protein structure to explain why (3)

A

Specific primary structure which leads to
Specific tertiary structure
So only complementary to one antigen

39
Q

Give two structures a bacterial cell may have that a white blood cell does not have (2)

A

Cell wall
Plasmid

Biology (33 decks)

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