Unit 4 Aos 1

• Antigens


  foreign molecules on the surface of the cell, will produce an immune response. Usually protein based, located on the plasma membrane of cells
• pathogens


  primary source of n on-self antigens which cause disease to the host
• cellular pathogens


  bacteria, fungi, oomycetes, protozoans, worms and arthropods
• Non-cellular pathogens


  viruses, viroids, prions
• Bacteria


  prokaryotic cells
• viruses


  genetic material with a protein coat, not living
• innate immune defences


  body already has them, provides broad protection against pathogens, non-specific defence mechanism
• adaptive immune defences


  mechanisms for specific antigens and pathogens
• innate immunity: physical barriers

  Epithelial tight junctions (our skin as a continuous barrier)
• innate immunity: chemical barrier

  mucus, secreted from membrane of certain cells, it can trap pathogens
• innate immunity: microbiological
• physical plant barriers


  bark prevents pathogens from entering trees, stomata close, leafs orientation ensures water doesn't collect and pathogens don't gather
• chemical barriers in animals

  tears, sweat, saliva: have enzymes which destroy the cell wall; stomach acid, surfactants
• chemical barriers in plants


  depends on plant: can be caffeine in insects and fungi or chitinase,
• second line of defence

  non-specific, rapid, present in all animals, fixed response, does not lead to the immune system remembering pathogen, cells of innate immune system
• PAMPs (pathogen-associated molecular patterns)

  molecules or structures not shared by the body's own cells, not specific to one pathogen
• TLRs (Toll like receptors)


  Receptors on phagocytic cells recognize PAMPs (molecules specific to a broad range of pathogens)
• phagocytes


  engulf and break down pathogens through the process of phagocytosis: macrophages, dendritic cells, neutrophils, monocytes (become macrophages or dendritic cells)
• Process of phagocutosis


  1. TLRs interact with PAMPS- activates the phagocyte

  2. Phagocyte engulfs pathogen, phagosome (plasma membrane) forms around pathogen

  3. inside the phagocyte, lysosome fuses with phagosome and injects digestive enzymes which break down the pathogen

  4. remains are then expelled via exocytosis or placed on surface of the phagocyte
• process of antigen presenting

  antigen presenting cells hold fragments of the antigen on the surface of a cell using major histocompatibility complex proteins. The presentation of non-self antigens shows the helper T-cells a foreign cell is present and results in its activation and release of cytokines (trigger greater immune response)
• MHC-1 proteins


  every cell must constantly show what proteins are being produced inside using MHC-1 proteins. If the body is infected, non-self antigens will be shown activating the cytotoxic T-cell. The cytotoxic T-cell then releases toxic chemicals which cause cell apoptosis.
• natural killer cells (NK cells)


  absence of of MHC-1 protein, triggers NK cells to kill infected, possibly cancerous, cells
• MHC-2 protein (not every cell)

  usually found on phagocytes like macrophages and dendritic cells; this is here antigen remains are placed, helper T-cells recognise the foreign cells and activate
• complement proteins


  activated when a pathogen is encountered, a cascade effect ensues = surrounding complement proteins are activated; the process of opsonization, increases the visibility of pathogen for phagocytes; puncture holes in the pathogen enabling enzymes from the lysosome to enter the pathogen and cause lysis
• cytokines


  signalling molecules of immune system
• cytokines: chemokines


  chemicals which attract leukocytes to site of infection - chemotaxis: use chemical gradient as pathway for leukocytes to site of infection
• Cytokines: Interferons


  chemicals released by virus-infected cell which act upon the same cell or those around it, to produce enzymes which break down viral RNA and attract NKs
• inflammation


  occurs when tissue in the body is damaged or infected, resulting in the accumulation of fluid, plasma, proteins and leukocytes. Cytokines released help attract immune cells to the site - specifically, neutrophils and mast cells (macrophages can also gather at site to secrete cytotoxins and aid neutrophils)
• mast cells


  release histamine
• histamine


  Chemical stored in mast cells that triggers dilation and increased permeability of capillaries - more complement proteins and platelets can enter infection site
• neutrophils (not antigen-presenting)


  phagocytes which engulf the pathogen at site of infection, can release chemicals which help kill pathogens
• pus


  collection of = leukocytes, dead pathogens and any cell debris
• Fever


  inflammatory cytokines act upon hypothalamus gland (regulates body temp) to increase body temp from 37 degree to slow pathogen process (e.g. replication) and speed up leukocyte activity
• third line of defence: adaptive immunity


  recognises and responds to specific antigens, consists of immunological memory. 2 types: humoral (B-cells) and cell-mediated (T-cells)
• B-cells


  produced in bone marrow, have surface antibodies (Receptors) which bind to antigens on pathogens, then differentiate and divide - cytokines can also help activate. 2 types
• plasma cells (b-cells)


  produce antibodies specific to antigen at a very fast rate
• memory b-cells


  retain antibodies on their surface and remain within lymphoid tissue for long periods of time - sometimes a lifetime - if a second response occurs, memory b-cells can divide and give rise to plasma cells
• Process of B cell activation

  1. B-cell comes into contact with an antigen complementary to antibody shape, the b-cell then ingests the pathogen

  2. B-cell displays antigen on MHC-2 protein marker

  3. helper t-cell which has been exposed to the same pathogen binds to the MHC-2 marker and recognises the foreign antigen

  4. Helper t-cell releases cytokines onto B-cell, causing proliferation and differentiation
• antibodies


  immunoglobins (Ig) protein structures produced and released into blood and lymph by b-cells. Can bind to specific antigens. Have a distinctive Y shape, variable region and constant region - variable region is complementary to specific antigen shape (binding area), constant region is able to attach to other parts of the immune system. Long chains and short chains. Do not destroy pathogens, they hinder effectiveness and increase efficiency of immune response
• antibodies: neutralisation of toxins


  bind to active site of toxic antigens and blocking their action, antigens are used t o enter host-cell, binding prevents antigen from performing tasks