immunology

• Antigen


  a protein molecule that stimulates an immune response resulting in the production of specific antibodies
• pathogens


  microorganisms that cause diseases by :

  - damaging body cells

  - releasing toxins that damage body cells
• non specific immune response


  immediate and same for all pathogens

  1. physical barrier

  2. phagocytosis
• physical barriers


  lungs - mucus membrane

  oesophagus - cilia

  lysozymes (hydrolytic enzymes) in tears and saliva

  skin
• phagocytosis - DIPFDD


  Detection - phagocyte detects the pathogen as attracted to chemicals release

  Ingestion - phagocyte engulfs pathogen

  Phagosome forms

  Fuses with lysosome containing lysosymes forming phagolysosome

  Digestion - lysozymes hydrolyse the pathogens

  Discharge - waste released (some antigens presented on cell) exocytosis
• Antigen Presenting cells


  phagocyte present antigens on its cell membrane become APC which can bring about SPECIFIC immune response
• Antibody


  a protein with a variable region has specific amino acid sequence. the tertiary structure of the binding site is complementary to antigens.

  produced by plasma cells
• Antigen- Antibody complexes.


  Antibody binding site is complementary to antigen to form an antigen antibody complexes. this lead to agglutination and phagocytes may then digest many pathogens at the same time.
• Cell mediated response


  T cells bind to antigen presenting cell and activates

  T cell divides by mitosis/ clonal selection

  cells differentiate into = cytotoxic T cells, or T helper cells

  Cytotoxic T cells = release perforin that puts holes into cell membrane

  T helper cells = activate B cells
• Humoral response


  T helper cells stimulate B cells

  B cell divides by mitosis/ clonal selection

  differentiate into plasma cells or memory cells

  plasma cells = release antibodies specific to antigen to destroy pathogens

  memory cells = stay in body in case of future infection by the same pathogen with same antigen
• secondary immune response


  the activation of memory cells to produce antibodies = secondary

  SIR is when the body is exposed to same a pathogen with the same antigens a 2nd time

  memory cells makes secondary immune response both quicker and produces more antibodies , more extensive
• antigenic variability


  when antigens mutate and change shape, making it difficult to develop vaccines against these pathogens

  when this occurs the receptors on memory cell dont recognise the pathogen

  the antibodies are no longer complimentary

  so have to go through specific and non specific immune response again = longer process
• types of immunity


  active and passive
• active immunity


  in response to an infection or vaccination

  exposed to antigen

  memory cells produced

  antibodies produced

  long term

  slow acting (has to go through full primary immune response)
• passive immunity


  after you receive antibodies from someone or somewhere

  no exposure to antigen

  no memory cells

  antibodies from outside the body

  short term

  fast acting
• Vaccine


  contains antigens from a dead or weakened pathogen to stimulate the production of antibodies and memory cells

  vaccines are not effective against pathogens that show antigenic variability
• vaccine process


  1. vaccine contains antigen from pathogen

  2. displayed on APC

  3. T cell binds to antigen on APC & activates

  4. divides by mitosis into t helper

  6. T helper stimulates B cells

  7. B cell divides by mitosis to give plasma cells

  8. Plasma cell produces/ secretes antibody

  9. antibodies destroy pathogens

  Upon reinfection - memory cells allow for rapid production of antibodies
• vaccination ethics


  cause side effects

  autonomy - decision of individual

  devlopment and testing on animals = infringe rights of animals?

  available to everyone or just those who can afford it?

  loss of genetic variability

  human testing = who should be tested/ is it a risk?
• HIV


  viral replication -

  viral proteins bind to receptors on t helper cell

  membranes fuse

  reverse transcriptase creates viral rna in dna

  viral dna integrates with host dna

  transcription and translation occurs creating viral proteins

  proteins appear on t helper cell surface

  reassembly of virus

  budding occurs
• what happens to t helper cells because of HIV


  t helper cell numbers decrease overtime

  therefore humoral response can not occur so no antibodies can be prodced

  the immune system is then weakened
• AIDS (acquired immune deficiency syndrome)


  symptoms are - low numbers of T helper cells

  one or more infections

  increase risk of developing cancer

  severe body wasting

  and can lead to death
• monoclonal antibodies


  made by the same B cell so are all sepcific to one type of antibody

  used for - research, immunoassays
• monoclonal antibodies in cancer treatment


  be made t bind to antigens of blood clots/ cancer cells

  easy to see where they have built up in the body

  attach to specific proteins produced by cells

  cancer cells have diff proteins on surface to non cancer cells

  comp antibodies to cancers can also have anti cancer drugs on the surface

  fewer side effects as only target cancer cells not nncancerous cells
• monoclonal antibodies in pregnancy tests


  complimentary to hcg hormone

  if pregnant then woman will have hcg hormones

  MA can bind to hcg and see if your pregnant
• ELISA (enzyme-linked immunosorbent assay)


  used to detect and quantify substance

  1. coat the well with antigen

  then wash to remove any unbound antigen

  2. add patients blood sample and if infected with specific pathogen they will hhave produced antigen- antibody complexes

  then wash to remove blood plasma and unbound antibody

  3. add enzyme linked antibody that will bind to already binded antibody

  then wash to remove any unbound enzyme linked antibody

  4. add substrate and if A-A complexes are present the enzyme on the enzyme linked atibody will cause substrate to change colour