specific immune response

• Antibodies 


  = Y- shaped glycoproteins called immunoglobins, which bind to a specific antigen on a pathogen that has triggered the immune response.
• antibody

  -made up of 2 identical long polypeptide chains= heavy chains and 2 shorter chains= light chains

  • held by disulfide bridges
  • can bind to 2 antigen binding sites at once
  • hinge region= provides flexibility, so it can bind to 2 antigens.
  • variable portion= binds to antigen, differs between antibody so can bind to different antigens.
  • constant portion= some in every antibody, phagocyte will bind, can be recognised.
  • when antibody binds to antigen it forms an antigen-antibody complex.
• antibody diagram

  
• how antibodies defend the body

  -opsinisation= tags pathogens

  -agglutination= causes pathogens to clump together and prevent them spreading through the body

  -antitoxins= neutralise pathogens
• B-lymphocytes

  = made and mature in bone marrow

  • plasma cells= produce antibodies to a particular antigen.
  • B effector cells= divide to form plasma cell clones.
  • B memory cells= provide immunological memory- remember a specific antigen+ enable body to make a rapid response.
• T- lymphocytes 


  • T helper cells= CD4 receptors on cell-surface membranes which bind to antigens. -Produce interleukins= stimulate activity of B cells so increases production of antibodies.
  • T killer cells= Produce perforin= kills pathogen, holes in membrane.
  • T memory cells= part of immunological memory- if meet antigen again they divide rapidly to form large numbers of T killer cells.
  • T regulator cells= supress the immune system- control+ regulate it. Stop immune system once pathogen is eliminated to ensure body recognises self antigens so no autoimmune response.
• T- lymphocytes

  = made in bone marrow, mature in thymus gland.
• Cell- mediated immunity

  -T lymphocytes respond to pathogens inside the cell.

  1. non-specific defence, macrophages engulf and destroy pathogens and form antigen presenting cells.
  2. receptors on T-helper cells fit antigens- produce interleukins- signal for more T cells to divide by mitosis (clonal expansion)
  3. differentiate to form: T-memory cells, T-killer cells, T-helper cells, regulatory cells.
• Humoral immunity

  = antigens found outside the cells

  -B lymphocytes

  • B cells display antigens
  • activated T-helper cells bind to B-cells (clonal selection) releases interleukins- signal B-cells to clone itself by mitosis
  • these B-cells differentiate to form plasma cells- release antibodies and memory cells. (clonal expansion)
• Autoimmune disease

  = sometimes the immune system stop recognising 'self' cells and starts to attack healthy body tissue.

  • some cases T-regulatory cells don't work properly
  • can cause chronic inflammation or complete breakdown and destruction of healthy tissue.
  • immunosuppressant drugs may be used as treatments- but can deprive the body of it's natural defences against communicable diseases.
• Examples of autoimmune disease

  -type 1 diabetes= insulin secreting cells in pancreas doesn't work.- treatment= insulin injections, pancreas transplant, immunosuppressant drugs.

  -Rheumatois arthiritis= joints (hands, feet, wrists, ankles)- no treatment= anti-inflammatory drugs, pain relief, immunosuppressant drugs.

  -lupus= affects skin and joints, can attack any organ in the body- no cure, anti-inflammatory and immunosuppressant drugs.
• • natural (encountering pathogen) vs artificial (not encountering)

  • active (own WBC- antibodies) vs passive (someone else WBC)
  • natural active= memory cells produce antibodies to destroy pathogen.
  • natural passive= antibodies pass form mother to baby/fetus across placenta/ in breast milk
  • artificial active= vaccination cause primary response allowing secondary response later.
  • artificial passive= antibodies taken from 1 organism, injected into another.

  Immune response
• secondary immune response

  produce more antibodies faster and for longer.