2.4 cell recognition and the immune system

• what is an antigen

  foreign molecule/protein/glycoprotein/glycolipid

  that simulates an immune response leading to production if antibody
• how are cells identified by the immune system

  each type of cell has specific molecule on its surface (cell-surface membrane/cell wall) that identify it

  often proteins that have a specific tertiary structure (or glycoproteins/glyocolipids)
• what types of cells and molecules can the immune system identify

  pathogens (disease causing microorganisms) e.g viruses, fungi and bacteria

  cells from other organisms of the same species (e.g from organ transplants)

  abnormal body cells (e.g tumour cells or virus infected cells)

  toxins (poisons) released by some bacteria
• describe phagocytosis of pathogens (non-specific immune response)

  phagocyte attracted by chemicals/recognises (foreign) antigens on pathogen

  phagocyte engulfs pathogen by surrounding it with its cell membrane

  pathogen contained in vesicle/phagosome in cytoplasm of phagocyte

  lysosome fuses with phagosome and releases lysozymes (hydrolytic enzymes)

  lysozymes hydrolyse/digest pathogen

  phagocytosis leads to presentation of antigens where antigens are displayed on the phagocyte cell-surfaced membrane, stimulating the specific immune response (cellular and humeral response)
• describe the response of T lymphocytes to a foreign antigen (the cellular response)

  T lymphocytes recognise (antigens on surface of) antigen presenting cells e.g infected cells, phagocytes, presenting antigens, transplanted cells and tumour cells ect

  specific helper T cells with complementary receptors (on cell surface) bind to antigen on antigen-presenting cell so activated and divide by mitosis to form cones which stimulate:

  cytotoxic T cells which kill infected cells/tumour cells (by producing perforin)

  specific B cells (humoral response)

  phagocytes which engulf pathogens by phagocytosis
• describe the response of B lymphocytes to a foreign antigen (the humoral response)

  B lymphocytes can recognise free antigens e.g blood or tissues not just antigen presenting cells

  clonal selection:

  specific B lymphocyte with complementary receptor (antibody on cell surface) binds to antigen

  this is then stimulated by helper T cells (which releases cytokines)

  so divides (rapidly) by mitosis to form clones

  some differentiate into B plasma cells which secrete large amounts of monoclonal antibody

  some differentiate into B memory cells which remain in blood for secondary immune response
• what are antibodies

  quaternary structure proteins (4 polypeptide chains)

  secreted by B lymphocytes e.g plasma cells in response to specific antigens

  bind specifically to antigens forming antigen-antibody complexes
• describe the structure of an antibody

  antigen

  antigen binding site

  variable region

  constant region

  disulfide bridge

  light polypeptide chain

  hinge region

  heavy polypeptide chain
• 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
• primary immune response

  primary - first exposure to antigen

  antibodies produced slowly and at a lower concentration

  takes time for specific B plasma cells to be stimulated to produce specific antibodies

  memory cells produced
• secondary immune response

  secondary - second exposure to antigen

  antibodies produced faster and at a higher concentration

  B memory cells rapidly undergo mitosis to produce many plasma cells which produce specific antibodies
• what is a vaccine

  injection of antigens from attenuated (dead or weakened) pathogens

  stimulating formation of memory cells
• explain how vaccines provide protection to individuals against disease

  specific B lymphocyte with complementary receptor binds to antigen

  specific T helper cell binds to antigen presenting cell and stimulates B cell

  B lymphocyte divides by mitosis to form clones

  some differentiate into B plasma cells which release antibodies

  some differentiate into B memory cells

  on second exposure to antigen B memory cells rapidly divide by mitosis to produce B plasma cells

  these release antibodies faster and at a higher concentration
• explain why vaccines provide protection for populations against disease

  herd immunity were a large proportion of population vaccinated which reduces spread of pathogen

  large proportion of the population immune so do not become ill form infection

  fewer infected people to pass pathogen on/unvaccinated people less likely to come in contact with someone with disease
• active immunity

  initial exposure to antigen e.g vaccine or primary infection

  memory cells involved

  antibody produced and recreated by B plasma cells

  slow so takes longer to develop

  long term immunity as antibody can be produced in response to a specific antigen again
• passive immunity

  no exposure to antigen

  no memory cells involved

  antibody introduced from another organism e.g breast milk/across placenta from mother

  faster acting

  short term immunity as antibody hydrolysed (endo/exo/dipeptidases)
• 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
• describe the structure of HIV

  lipid envelope

  RNA

  reverse transcriptase

  capsid

  attachment protein
• describe the replication of HIV in helper T cells

  HIV attachment proteins attach to receptors on T helper cells

  lipid envelope fuses with cell-surface membrane relating capsid into cell

  capsid uncoats releasing RNA and reverse transcriptase

  reverse transcriptase converts viral RNA to DNA

  viral DNA incorporated/inserted into helper T cell DNA (may remain latent)

  viral protein/caspid/enzyme produced

  DNA transcribed into HIV mRNA

  HIV mRNA translated into new HIV proteins

  virus particles assembled and released from cell (via budding)
• explain how HIV causes the symptoms of acquired immune deficiency syndrome (AIDS)

  HIV infects and kills helper T cells (host cell) as it multiples rapidly

  so T helper cells cant stimulate cytotoxic T cells, B cells and phagocytes

  so B plasma cells can't release as many antibodies for agglutination and destruction of pathogens

  immune system deteriorates so 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 (e.g do not make protein)/ribosomes

  viruses do not have bacterial cell 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 (e.g cancer)

  therapeutic drug attached to antibody

  antibody binds to specific cell forming antigen-antibody complex, delivering drug
• explain how monoclonal antibodies can be used in medical diagnosis

  monoclonal antibody has a specific tertiary structure/binding site/variable region

  complementary to a specific receptor/protein/antigen associated with diagnosis

  dye/stain/florescent marker attached to antibody

  antibody binds to receptor/protein/antigen forming an antigen-antibody complex
• (DIRECT ELISA)

  attach sample with potential antigens to well

  add complementary monoclonal antibodies with enzymes attached so bind to antigens if present

  wash well to remove unbound antibodies (to prevent false positive)

  add substrate so enzymes create products that causes a colour change (positive result)
• (SANDWICH ELISA)

  attach specific monoclonal antibodies to well

  add sample with potential antigens then wash well

  add complementary monoclonal antibodies with enzyme attached so bind to antigens is present

  wash well to remove unbound antibodies (to prevent false positive)

  add substrate so enzymes create products that cause a colour change (positive result)
• (INDIRECT ELISA)

  attach specific antigens to well

  add sample with potential antibodies and wash well

  add complementary monoclonal antibodies with enzyme attached to bind to antibodies if present

  wash well to remove unbound antibodies

  add substrate so enzymes create products that cause colour change (positive result)
• suggests 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
• discuss some general ethical issues associated with the use of vaccines and monoclonal antibodies

  pre-clinical testing on/use of animals so potential stress/harm/mistreatment

  but animals not killed and helps produce new drugs to reduce human suffering

  clinical trials on humans so potential harm/side effects

  vaccines so may continue high risk activities and still develop/pass on pathogen

  use of drug so potentially dangerous side effects