cell recognition and the immune system

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

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

What is an antigen?

Foreign proteins on the cell- surface membrane

trigger an immune response when detected by lymphocytes

leading to production of antibody

Antigenic

variability

When pathogenic DNA mutates, causing a change in shape to then antigen

previous immunity is no longer effective as memory B cells do not recognise the altered shape of the antigen.

specific antibody no longer binds to new antigen

How are cells identified by the immune system?

● 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)

Describe phagocytosis of pathogens (non-specific immune response)

Describe the response of T lymphocytes to a foreign antigen (the cellular response)

Describe the response of B lymphocytes to a foreign antigen (the humoral response)

What are antibodies?

Explain how antibodies lead to the destruction of pathogens

● 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

Explain the differences between the primary & secondary immune response

● 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

What is a vaccine?

● Introduction (eg. injection) of antigens → could be from attenuated (dead / weakened) pathogens

● Stimulating formation of memory cells

Explain how vaccines provide protection to individuals against disease

Explain how vaccines provide protections for populations against disease

Describe the differences between active and passive immunity

Explain the effect of antigen variability on disease and disease prevention

● 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

Example applications: yearly new flu vaccines developed, no vaccine for HIV, can catch a cold many times

Describe the structure of a HIV particle

Describe the replication of HIV in helper T cells

Explain how HIV causes the symptoms of acquired immune deficiency

syndrome (AIDS)

● 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

Explain why antibiotics are ineffective against viruses

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

What is a monoclonal antibody?

● Antibody produced from genetically identical / cloned B lymphocytes / plasma cells

● So have same tertiary structure

Explain how monoclonal antibodies can be used in medical treatments

● Monoclonal antibody has a specific tertiary structure / binding site / variable region

● Complementary to receptor / protein / 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.

Explain how monoclonal antibodies can be used in medical diagnosis

● 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.

Explain the use of antibodies in the ELISA (enzyme-linked immunosorbent

assay) test to detect antigens

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

Suggest the purpose of a control well in the ELISA test

● Compare to test to show only enzyme causes colour change

● Compare to test to show all unbound antibodies have been washed away

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

in the ELISA test

● Antibody with enzyme remains / not washed out

● So substrate converted into colour product

Suggest some general ethical issues associated with the use of vaccines

and monoclonal antibodies

● Pre-clinical testing on / use of animals → potential stress / harm / mistreatment

○ But animals not killed & helps produce new drugs to reduce human suffering

● Clinical trials on humans → potential harm / side-effects

● Vaccines → may continue high risk activities and still develop / pass on pathogen

● Use of drug → potentially dangerous side effects

Suggest some points to consider when evaluating methodology relating to

the use of vaccines and monoclonal antibodies

● Was the sample size large enough to be representative?

● Were participants diverse in terms of age, sex, ethnicity and health status?

● Were placebo / control groups used for comparison?

● 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?

Suggest some points to consider when evaluating evidence and data

relating to the use of vaccines and monoclonal antibodies

● 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?

● 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?

● What dosage was optimum? Does increasing dose increase effectiveness enough to justify extra cost?

● Was the cost of production & distribution low enough?

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