topic 2C: cells and the immune system

Question 1

antigen definition

Answer 1

● Foreign molecule / protein / glycoprotein / glycolipid
● That stimulates an immune response leading to production of antibody

Question 2

how are cells identified by the immune system?

Answer 2

● Each type of cell has specific molecules on its surface (cell-surface membrane / cell wall) that identify it
● Often proteins → have a specific tertiary structure (or glycoproteins / glycolipids)

Question 3

what types of cells and molecules can the immune system identify?

Answer 3

1. Pathogens (disease causing microorganisms) eg. viruses, fungi, bacteria
2. Cells from other organisms of the same species (eg. organ transplants)
3. Abnormal body cells eg. tumour cells or virus-infected cells
4. Toxins (poisons) released by some bacteria

Question 4

describe the two different parts of the immune system

Answer 4

NON SPECIFIC immune response: phagocytosis and physical barriers (skin, mucus)

SPECIFIC immune response: T and B lymphocytes - cellular and humoral response

Question 5

phagocyte

Answer 5

a phagocyte (e.g. macrophage) is a type of white blood cell that carries out phagocytosis (engulfment of pathogens). They are found in the blood and in tissues and the first cells to respond to an immune system trigger inside the body - they carry out a non specific immune response.

Question 6

1. describe phagocytosis of pathogens + antigen presenting cells

Answer 6

-the phagocyte (e.g. macrophage) recognises and binds to the foreign antigens on a pathogen
-the phagocyte ENGULFS the pathogen by surrounding it with its cell membrane
-the pathogen is contained within a PHAGOSOME VESICLE in the cytoplasm of the phagocyte
-a lysosome (contains enzymes called lyzozomes) fuses with the phagosome vesicle and releases lyzozymes (hydrolytic enzymes)
-the lyzozymes hydrolyse the pathogen

-phagocytosis leads to presentation of antigens where antigens are displayed on the phagocytes CELL SURFACE MEMBRANE, stimulating and activating the SPECIFIC immune response - either cellular and humoral response

Question 7

2. describe the response of T lymphocytes (T-cells) to a foreign antigen (cellular response) + types of different cells produced

Answer 7

T lymphocytes recognise (antigens on surface of) antigen presenting cells eg. infected cells, phagocytes presenting antigens, tumour cells etc.

-a specific HELPER T-CELLS have a complementary receptor protein on the cell surface which binds to an antigen on an antigen presenting cell
-this ACTIVATES the helper t-cell to divided rapidly by mitosis and form clones WHICH STIMULATE:
● Cytotoxic T cells → kill infected cells / tumour cells (by producing perforin)
● Specific B cells (humoral response - see below)
● Phagocytes → engulf pathogens by phagocytosis

Question 8

3. describe the response of B lymphocytes to a foreign antigen (the humoral response) + what is clonal selection? UPTO MOCK

Answer 8

B lymphocytes can recognise free antigens eg. in blood or tissues, not just antigen presenting cells.

1. CLONAL SELECTION
   -a specific B lymphocyte with a complementary receptor (antibody on cell surface membrane) binds to an antigen
   -this is then ACTIVATED by the cytokines released by a specific helper T-cell
   -so divides rapidly by mitosis to form clones which differentiate into:
2. -B plasma cells: secretes large amounts of (monoclonal) antibodies
3. -B memory cells: remain in the blood for secondary immune response

Question 9

4. role of B plasma cells + B memory cells

Answer 9

B PLASMA CELLS (slower + short lived - primary immune response)
-plasma cells produces and secretes large amounts of monoclonal antibodies, which are specific to the antigen

B MEMORY CELLS (faster + long lasting - secondary immune response)
-remain in the body (blood) for secondary immune response
-memory B cells divide by mitosis and produces plasma cells which release more antibodies more rapidly after the second exposure to the same antigen

Question 10

antibody definition

Answer 10

-antibodies are quaternary structure PROTEINS (4 polypeptide chains), secreted by B lymphocytes (e.g. plasma cells in response to specific antigens), they bind specifically to antigens forming antigen-antibody complexes

Question 11

antibody structure

Answer 11

-Quaternary structure proteins (4 polypeptide chains)
-the specificity of an antibody depends on its VARIABLE REGIONS, which form the antigen binding sites

-each antibody has a VARIABLE REGION with a unique tertiary structure (due to different sequence of amino acids) that’s complementary to one specific antigen
-all antibodies have the same CONSTANT REGION (doesn’t change)
-2 SHORT (light) CHAINS + 2 LONG (heavy) CHAINS

Question 12

explain how antibodies lead to the destruction of pathogens

Answer 12

● Antibodies bind to antigens on pathogens forming an antigen-antibody complex
○ Specific tertiary structure so binding site / variable region binds to complementary antigen
● Each antibody binds to 2 pathogens at a time causing agglutination (clumping) of pathogens
● Antibodies attract phagocytes
● Phagocytes bind to the antibodies and phagocytose many pathogens at once

Question 13

Explain the differences between the primary & secondary immune response

Answer 13

● Primary - first exposure to antigen
○ Antibodies produced slowly & at a lower conc.
○ Takes time for specific B plasma cells to be
stimulated to produce specific antibodies
○ Memory cells produced

● Secondary - second exposure to antigen
○ Antibodies produced faster & at a higher conc.
○ B memory cells rapidly undergo mitosis to
produce many plasma cells which produce
specific antibodies

Question 14

vaccine definition

Answer 14

-an injection of antigens from a dead pathogen, stimulating the production of memory cells

Question 15

explain how vaccines provide protection to individuals against disease

Answer 15

1. Specific B lymphocyte with complementary receptor binds to antigen
2. Specific T helper cell binds to antigen-presenting cell and stimulates B cell
3. B lymphocyte divides by mitosis to form clones
4. Some differentiate into B plasma cells which release antibodies
5. Some differentiate into B memory cells
6. On secondary exposure to antigen, B memory cells rapidly divide by mitosis to produce B plasma cells
7. These release antibodies faster and at a higher concentration

Question 16

Explain how vaccines provide protections for populations against disease

Answer 16

● Herd immunity - large proportion of population vaccinated, reducing spread of pathogen
○ Large proportion of population immune so do not become ill from infection
○ Fewer infected people to pass pathogen on / unvaccinated people less likely to come in contact
with someone with disease

Question 17

active immunity

Answer 17

-Initial exposure to antigen eg. vaccine or primary infection
-Memory cells involved
-Antibody produced and secreted
by B plasma cells
-Slow; takes longer to develop
-Long term immunity as antibody can be produced in response to a specific antigen again

Question 18

passive immunity

Answer 18

-No exposure to antigen
-No memory cells involved
-Antibody introduced from another organism eg. breast milk / across placenta from mother
-Faster acting
-Short term immunity as antibody hydrolysed (endo/exo/dipeptidases)

Question 19

Explain the effect of antigen variability on disease and disease prevention

Answer 19

● Antigens on pathogens change shape / tertiary structure due to gene mutations (creating new strains)
● So no longer immune (from vaccine or prior infection)
○ B memory cell receptors cannot bind to / recognise changed antigen on secondary exposure
○ Specific antibodies not complementary / cannot bind to changed antigen

Question 20

HIV definition + causes

Answer 20

HIV (human immunodeficiency virus) is a virus that affects the human immune system - it eventually leads to AIDS

Question 21

structure of HIV

Answer 21

-a spherical structure which contains:
-a core that contains the GENETIC MATERIAL (RNA) and some PROTEINS which are the ENZYME REVERSE TRANSCRIPTASE, which is needed for virus replication - (HIV cannot replicate itself)
-LIPID ENVELOPE - membranes stolen from the cell membrane of a previous host cell
-CAPSID - outer protein coat (enzyme reverse transcriptase)
-ATTACHMENT PROTEIN - sticking out of the envelope, helps HIV attach to the host helper T-cell

Question 22

Describe the replication of HIV in helper T cells

Answer 22

1. HIV attachment proteins attach to receptors on helper T cell
2. Lipid envelope fuses with cell-surface membrane, releasing capsid into cell
3. Capsid uncoats, releasing RNA and reverse transcriptase
4. Reverse transcriptase converts viral RNA to DNA
5. Viral DNA inserted / incorporated into helper T cell DNA (may remain latent)
6. Viral protein / capsid / enzymes are produced
   a. DNA transcribed into HIV mRNA
   b. HIV mRNA translated into new HIV proteins
7. Virus particles assembled and released from cell (via budding)

Question 23

Explain how HIV causes the symptoms of acquired immune deficiency
syndrome (AIDS)

Answer 23

● HIV infects and kills helper T cells (host cell) as it multiplies rapidly
○ So T helper cells can’t stimulate cytotoxic T cells, B cells and phagocytes
○ So B plasma cells can’t release as many antibodies for agglutination & destruction of pathogens
● Immune system deteriorates → more susceptible to (opportunistic) infections
● Pathogens reproduce, release toxins and damage cells

Question 24

Explain why antibiotics are ineffective against viruses

Answer 24

Viruses do not have structures / processes that antibiotics inhibit:
● Viruses do not have metabolic processes (eg. do not make protein) / ribosomes
● Viruses do not have bacterial enzymes / murein cell wall

Question 25

What is a monoclonal antibody?

Answer 25

-Antibody produced from genetically identical B lymphocytes (plasma cells), so they have same tertiary structure

Question 26

Explain how monoclonal antibodies can be used in medical treatments

Answer 26

Monoclonal antibody has a specific tertiary structure / binding site -Complementary to antigen found only on a specific cell type (eg. cancer cell) -Therapeutic drug attached to antibody -Antibody binds to specific cell, forming antigen-antibody complex, delivering drug Some monoclonal antibodies are also designed to block antigens / receptors on cells

Question 27

Explain how monoclonal antibodies can be used in medical diagnosis

Answer 27

● Monoclonal antibody has a specific tertiary structure / binding site / variable region ● Complementary to specific receptor / protein / antigen associated with diagnosis ● Dye / stain / fluorescent marker attached to antibody ● Antibody binds to receptor / protein / antigen, forming antigen-antibody complex Examples vary, eg. pregnancy tests - you’ll need to interpret information in the question on how these work

Question 28

what are the two types of ELISA tests?

Answer 28

DIRECT ELISA: uses a single antibody that is complementary to the antigen you're testing for INDIRECT ELISA: different because it uses two different antibodies

Question 29

Explain the use of antibodies in the ELISA test to detect ANTIGENS - direct elisa

Answer 29

direct ELISA - testing for antigens using a known antibody 1. Attach sample with potential antigens to well 2. Add complementary monoclonal antibodies with enzymes attached → bind to antigens if present 3. Wash well → remove unbound antibodies (to prevent false positive) 4. Add substrate → enzymes create products that cause a colour change (positive result)

Question 30

Explain the use of antibodies in the ELISA (enzyme-linked immunosorbent assay) test to detect antigens - sandwich elisa

Answer 30

1. Attach specific monoclonal antibodies to well 2. Add sample with potential antigens, then wash well 3. Add complementary monoclonal antibodies with enzymes attached → bind to antigens if present 4. Wash well → remove unbound antibodies (to prevent false positive) 5. Add substrate → enzymes create products that cause a colour change (positive result)

Question 31

Explain the use of antibodies in the ELISA test to detect ANTIBODIES

Answer 31

Example method (indirect ELISA): 1. Attach specific antigens to well 2. Add sample with potential antibodies, wash well 3. Add complementary monoclonal antibodies with enzymes attached → bind to antibodies if present 4. Wash well → remove unbound antibodies 5. Add substrate → enzymes create products that cause a colour change (positive result)

Question 32

Suggest why failure to thoroughly wash the well can result in a false positive in the ELISA test

Answer 32

● Antibody with enzyme remains / not washed out ● So substrate converted into colour product

Question 32

Suggest the purpose of a control well in the ELISA test

Answer 32

● Compare to test to show only enzyme causes colour change ● Compare to test to show all unbound antibodies have been washed away

Question 33

Suggest some points to consider when evaluating methodology relating to the use of vaccines and monoclonal antibodies

Answer 33

-SAMPLE SIZE: Was the sample size large enough to be representative? --FACTORS WITHIN VOLUNTEERS AFFECTING: Were participants diverse in terms of age, sex, ethnicity and health status? -PLACEBO EFFECT: Were placebo / control groups used for comparison? -LONG TERM EFFECTS: Was the duration of the study long enough to show long-term effects? -Was the trial DOUBLE-BLIND (neither doctor / patient knew who was given drug or placebo) to reduce bias?

Question 34

Suggest some points to consider when evaluating evidence and data relating to the use of vaccines and monoclonal antibodies

Answer 34

-SIDE EFFECTS: What side effects were observed, and how frequently did they occur? -Was a statistical test used to see if there was a significant difference between start & final results? -STANDARD DEVIATIONS: Was the standard deviation of final results large, showing some people did not benefit? -Did standard deviations of start & final results OVERLAP, showing there may not be a SIGNIFICANT DIFFERENCE? -OPTIMUM DOSAGE: What dosage was optimum? Does increasing dose increase effectiveness enough to justify extra cost? -COST PRODUCTION + DISTRIBUTION: Was the cost of production & distribution low enough?