Topic 12

• Why are non specific defences classed as non specific?

  They are able to break down any type of pathogen as they do not have antigen-specific receptors.
• Explain the primary defence of skin

  A physical barrier to prevent entry of microorganisms:

  -Skin flora of healthy microorganisms that outcompete pathogens for space on the body surface

  -Produces sebum, that inhibits the growth of pathogens.
• Explain the primary defence of body tracts lined with mucous membranes.

  Many body tracts lined by mucous membranes, Secrete sticky mucus to trap pathogens:

  -Mucus contains lysozymes which destroy bacterial and fungal cell walls.

  -Mucus contains phagocytes which remove remaining pathogens.
• Explain the primary defence of the body with lysozymes in tears and urine

  Breaks down cell walls of fungal and bacterial cells.
• Explain the primary defence of stomach acid

  Destroys pathogens by lowering the pH in which bacteria cannot survive and reproduce in these conditions.
• Explain the primary defence of expulsive refluxes.

  Coughs and sneezes eject pathogenic mucus from the gas exchange system

  Vomitting and diarrhoea expel the contents of the guts and any pathogens.
• Explain the process of blood clotting.

  Platelets exposed to collagen in the wall of the blood vessel. Damaged blood vessel begins to adhere and secrete thromboplastin.

  THROMBOPLASTIN: triggers a cascade of reactions resulting in the formation of a blood clot.

  Prothrombin> thrombin, catalysed by thromboplastin and ca2+

  Soluble fibrinogens>Insoluble fibres, catalysed by thrombin

  Insoluble fibres form a mesh of fibres trapping cells and platelets, clot prevents bleeding and dries out forming a tough scab preventing entry of pathogens.

  Epidermal cells below scab start to grow . damaged blood vessels regrow and collagen is deposited

  Serotonin-Makes smooth muscle contract in the blood vessel walls so they narrow and reduce the blood supply to the area
• What is the inflammatory response?

  Localised response to pathogens causing inflammation at the site of the infection.

  -pain,heat,redness,swelling of tissue
• What causes sweling/redness?


  Mast cells are activated in the damaged tissue and release histamines and cytokines.

  
  

  Histamines: cause arterioles (blood vessels) to dilate and allow more blood to the area causing redness and localised heat.

  -Raise in temperature helps prevent pathogens reproducing.

  -Make blood vessel walls more leaky so blood plasma is forced out. Once blood plasma is forced out of the blood it forms tissue fluid. Formation of more tissue fluid causes swelling/oedema and pain

  
  

  Cytokines: Attract phagocytes to the area to dispose of pathogens by phagocytosis.
• What causes discomfort?


  Excess tissue fluid is drained to the lymph vessels as lymph, pathogens in the tissue fluid enter lymph fluid.

  1. Transported along lymph system in lymphnodes.

  2.Activity of phagocytes cause swelling of lymphnodes
• Once pathogens enter the body it is a secondary defence why?

  It is the response after the pathogen has entered the body- prevent them growing or destroy them
• Why are fevers a secondary defence?

  Cytokines stimulate hypothamalus to increase the body temp:

  High temp stops pathogens reproducing

  Specific immune system works better at higher temps
• The process of phagocytosis

  1.Pathogens produce chemicals that attract phagocytes.

  2.Phagocytes recognise non self proteins on the pathogen on the cell surface membrane and bind to it.

  3.Phagocyte engulfs the pathogen by phagocytosis and encloses it in a vaccuole called a phagosome.

  4.Lysosomes move towards phagosomes and fuse with eachother forming a phagolysosome.

  5.Enzymes from the lysosome digest and destroy the pathogen.
• How do the two different white blood cells break down the pathogen.

  Neutrophils- break down products absorbed into cytoplasm by diffusion

  Macrophages-Antigens from the pathogens cell surface membrane combine with the MHC (glycoprotein in macrophages cytoplasm)

  MHC complex move the pathogens antigens to the macrophages own cell surface membrane becoming an antigen presenting cell (APC)

  summary:

  Antigen presenting cell ingest antigens from pathogens and display it on their cell surface membranes.
• Helpful chemicals in phagocytosis:

  Cytokines: act as cell signalling molecules by attracting more phagocytes to the infected area, increase body temperature and stimulate the specific immune system.

  Opsonins: bind to antigen on pathogen and tag them so they are easily recognised by phagocytes. To increase the likelihood of phagocytosis

  Build up of phagocytes presents pus- dead neutrophils and pathogens.
• Why is the specific immune system classified as specific.

  Only able to break down a certain type of pathogen.

  The specific immune system takes much longer, but the immune memory cells mean the second invasion by the same pathogen is much quicker.
• What do non-self antigens trigger?

  Production of antibodies
• Explain the structure of an antibody.

  A Y shaped glycoprotein called immunoglobulin. Only bind to a specific antigen on the pathogen/toxin.

  - 2 light chains and 2 heavy chains, disulfide bridges hold together the polypeptide chains( light and heavy chains) together, disulfide bridges within the chains to hold them in shape.

  -Constant region is always the same, it allows binding to phagocytes

  -Hinge reigon allows flexibility and to bind to two seperate antigens

  -Variable reigon allows binding to antigen. There are two variable reigons to allow binding of more than one of the same antigen. Variable region is different on every antibody to give its specificity to different antigens.

  
  

  When an antibody binds to an antigen it forms an antigen-antibody complex, vr has 110 amino acids
• How do antibodies defend the body?

  1.Antibody of antigen-antibody complex acts as an opsonin so increases likelihood of phagocytosis.

  2.Act as agglutinins, causes pathogens carrying antigen-antibody complexes to clump together which allows phagocytes to engulf a large number of pathogens at the same time and makes them too big to enter and damage host cells.

  3.Antibodies act as anti toxins, binding to toxins produced making them harmless

  4.Once part of antigen-antibody complex pathogens can no longer effectively invade host cells.
• Where do t lymphocytes and b lymphocytes mature.

  T lymphocytes- thymus gland

  B lymphocytes- bone marrow
• Function of T Helper cells

  . Produce interleukins (a cytokine) which stimulate the activity of B cells ( increases antibody production, stimulates production of other types of T cells such as t memory cells, stimulates macrophages to ingest pathogens with antibody-antigen complexes.

  -Have CD4 receptors on cell surface membrane which bind to antigens on APCs
• Function of T Killer cells

  Produce Perforin which kills the pathogen by making holes in the cell membrane so it is freely permeable which kills the pathogen
• Function of T memory cells

  Part of the immunological memory (long life), Allow a fast secondary immune response by dividing rapidly to form clones of T Killer cells to destroy the pathogen.
• Function of T Regulator cells

  Suppress the immune system to control and regulate it. Stop the immune system once a pathogen has been eliminated:

  -Makes sure the body recognises self antigens

  -Makes sure the body doesnt set up an autoimmune response

  Interleukins important in this control.
• Function of Plasma cells (b-lymphocyte)


  Produce antibodies to paticular antigens and release them into circulation.
• B effector cells


  Divide to form plasma cell clones.
• B Memory cells


  Part of immunological memory (long life) programmed for a faster secondary response by remembering a specific antigen.
• Why is it called cell mediated immunity?

  Respond to altered cells such as antigens on APCS, cancers and viruses
• What is cell-mediated immunity

  1. Macrophages ingest antigens and process them to display them on their cell surface membranes.

  2.Receptors on T Helper cells bind to antigens on APC's.

  3.T helper cells become activated and produce interleukins which stimulate more T cells to divide by mitosis to form clones of identical activated T Helper cells

  4.Cloned T cells may:

  1.Develop into T memory cells

  2.Develop into T killer cells

  3.Porduce interleukins to stimulate phagocytosis.

  4.Produce interleukins to stimulate B cells to divide
• What is humoral immunity?

  Repsond to antigens found outside cells such as bacteria,fungi and APCS. Produce specific antibodies to the antigen
• Process of humoral immunity

  1. B lymphocytes with the specific antibody will bind to the specific antigen, it will ingest and process these antigens to become an APC by endocytosis.

  2. Activated T Helper cell binds to the B cell APC with the correct antibody for the specific antigen, (clonal selection) and is selected for cloning.

  3.Interleukins produced by the activated T Helper cell activate the B cells.

  4.Activated B cells undergo mitosis to give clones of plasma cells and B memory cells (clonal expansion)

  5.Cloned plasma cells produce antibodies that bind to the antigens and disable them or act as opsonins or agglutinins. (primary response- takes weeks which is why we get ill as the pathogen is reproducing)

  6.Cloned B cells differentiate into B memory cells (secondary response) if it comes across the same pathogen it divides to form plasma cell clones which produces the correct antibody for the specific antigen
• Primary response and secondary response difference.

  Primary is just after vaccination, slower response because of clonal selection and clonal expansion

  Secondary is much quicker as memory cells are present which divide rapidly to form plasma cells with the correct antibody for the specific pathogen
• Primary and secondary response

  Primary-Cloned plasma cells produce antibodies which bind to the antigen and disable them.

  Secondary- Cloned B cells differentiate into B memory cells which if it comes across the antigen divides to form plasma cell clones to produce antibodies.
• What is a autoimmune disease?

  An abnormal immune response against tissues normally in the body.

  Immune system stops recognising self cells and attack healthy body tissues.
• Examples of autoimmune diseases

  Rheumatoid arthiritis- affects joints no cure but anti-inflammatory drugs/steroids/immunosepreseants/pain relief helps.

  Lupus- affects skin/joints and can attack any organ no cure but steroids/anti-inflammatory drugs/immunosepressants help.

  Type 1 diabetes- affects insulin secreting cells in pancreas no cure but insulin injections/pancreas transplants/immunosupressant drugs help.
• Natrual active immunity


  When you meet a pathogen for the first time, the body acts itself to produce antibodies and memory cells which remain in the immunological memory
• Natrual passive immunity


  Milk from a mother contains colostrum which is high in antibodies, infant guts allow these antibody glycoproteins into the bloodstream.

  -some antibodies cross the placenta from the mother to the fetus so has some immunity at birth
• Artifical passive immunity


  Antibodies are formed in one individual and injected into the bloodstream of another individual only temporary immunity.
• Artificial active immunity


  Vaccinations as the immune system is stimulated to make its own antibodies to a safe form of an antigen which is injected into the bloodstream

  1. Vaccine is produced in a safe form of an antigen(killed/inactivated/attenuated meaning weakened/toxins altered and detoxified/genetically engineered antigens/isolate and extract antigens)

  2.Injected into the bloodstream of the individual.

  3. Antigen binds to B Cell, B cell ingests these and presents these antigens on their cell surface membrane to become an antigen presenting cell.

  4.Clonal selection Binds to activated T Helper cell which produces interleukins to activate B Cell APC.

  5. Clonal expansion activated B Cell divides rapidly to form identical B cell clones which differntiate into plasma cell clones.

  6.Produce antibodies which is primary response.

  7.Differntiate into B memory cells, secondary response which can divide to Plasma cells if come across pathogen again.
• Difference between epidemic and pandemic

  Epidemic- communicable disease spreads rapidly at a local/national level

  Pandemic- Communicable disease spreads rapidly at a international level