immunity goes wrong

• pattern recognition molecules play a key role in complement cascades
• 5 responses to injury/infection:

  • heat due to increased blood flow
  • redness due to increased blood flow
  • swelling due to increased permeability
  • pain due to stimulation of nerve ending bc of inflammation
  • loss of function to site of damage
• aquired immunity is expressed after exposure and mediated by lymphocytes
• lymphocytes are involved in the humoral and cell mediated immune response
• aquired immunity takes more time but is more specific
• aquired immunity can be active or passive
• antibody is a protective protein produced by the immune system when in the presence of an antigen
• antibodies recognise and bind to the antigen to remove it
• an antigen is any substance that is foreign to the body evoking an immune response
• an antibody can evoke an immune reponse alone or after forming a complex with a larger molecule which binds with a product of the imune repsonse
• autoantibodies are produced by the immune system which mistakely attack the body's own cells
• an autoimmune disease is a disease where the immune system attacks specific tissue and/or organs
• autoimmunity is when host immune systen attacks its own cells and organs instead of protecting them
• there are 4 types of hypersensitivity:

  • type 1: immediate
  • type 2: antibody-mediated cytotoxicity
  • type 3: immune complex mediated
  • type 4: delayed
• type 1 is an exaggerated response that is intiated by IgE which is rapid and onset associated with food allergies, asthma, allergic rhinitis and anaphlaxis
• symptoms of type 1 may include hey fever, hives, eczema along with several other sever reactions
• upon first exposure to allergen IgE is produced and subsequent exposure triggers release of histamines and other mediators form mast cells leading to the characterised symptoms that follow hypersensitivity
• in type 2 is caused by an Ab-Ag complex on cell and tissue surface causing damage to site due as IgG and IgM are directed to these areas and the cytotoxins released further cause damage
• type 2 hypersensitivity can occur as a result of complememnt activation, phagocytosis or cell lysis
• type 3 hypersensitivity is mediated by IgG/M and is caused by immune complexes which are deposited at tissues which then lead to inflammation and damge of these tissues
• complement actovation + inflammatory cells = tissue damage
• type 4 sensititivity occurs over hours to days after exposure ot the antigen with T cells playing the central role that mediates this reaction
• in type 4 after exposure to Ag sensitised T cell, the release of cytokines is intiated which can then attract inflammatory cells which can cause tissue damage