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Immune System immune_banner, Source: Abbas, Abul K.Lichtman, Andrew H.…

- - - - Release performs to create pores in cell and therefore permeable to water and ions, this will lead to swelling and bursting of the cell
      - The recognition of a to be killed cell is based on the absence of MHC-1
      - Destroy infected host cells to stop the infection from spreading
    - - Produce cytokines in reaction to microbes
      - Attract leukocytes and initiate adaptive immune system
    - - Important for wound healing and defensive against pathogens via inflammatory response
      - Release cytokines, granules and histamine to create inflammatory cascade
      - In mucous membranes and connective tissues
    - - Neutrophils
        
        Contain granules in cytoplasm, which are very toxic to bacteria and case them to stop proliferating or die on contact
        
        Arrive first at sit, because there are a lot present in circulation at any given time
        
        1st line phagocytic cells
      - Macrophages
        
        Hunt pathogens with less limits, because they can move outside the circulatory system
        
        Can release cytokines to recruit and signal other cells
        
        2nd line of phagocytic cells
        
        Activation
    - - Basophils
        
        Release histamines to mount an allergic response
      - Eosinophils
        
        Secrete toxic proteins and free radicals
  - - - Vasodilation
        
        Increased blood flow (Rubor Calor)
      - Walls of blood vessels become more permeable
        
        Exudation of fluid into tissue (tummy)
      - Blood flow changes
      - Adherence of WBC's to blood vessel wall
    - - Originate from blood plasma, WBC's, platelets, mast cells, vascular endothelium, damaged tissue cells.
      - Histamine (stored in mast cells and granules of basophils
        
        Triggers vasodilation and vascular permeability
      - TNF-a (secreted by macrophages)
      - Kinins, prostaglandins, complement, cytokines
      - lysosomal enzymes
    - - Cell migration of WBC
        
        Rolling (close rolling with close contact to endothelium
        
        Adhesion (connecting to the endothelium wall )
        
        Margination (cells line up against endothelium
        
        Emigration cells move through the vessel wall to affected area
      - accumulation of WBC's at site of injury
    - - Calor (heat)
      - Tumor (swelling)
      - Rubor (redness)
      - Pain (dolor)
  - - - C3b proteolysis
        
        MCP serves as cofactor
        
        CR1 serves as both mediator and cofactor
        
        Mediated by factor I
      - C1 INH stops C1
      - DAF disrupts binding of factor B/C4b2 to C3b
      - preventing MAC formation
    - - Induction of Inflammation
        
        Anaphylatoxins (C3a, C4a and C5a) are pro-Inflammatory
      - Cytolysis
        
        MAC Inserts into microbial cell membrane, disturbing permeability
        
        Apoptotic cell death
        
        Osmotic lysis
      - Opsonisation
        
        C3b that coats microbes binds to C3b receptors on phagocytes
    - - Classical Pathway
        
        Humoral adaptive immunity
        
        Activated when antibodies bind to antigens
      - Lectin Pathway
        
        Activated when MBL binds to surface glycoproteins of microbes
        
        Innate Immunity
      - Alternative Pathway
        
        Innate immunity
        
        Activated when complement proteins on microbial surfaces are activated
        
        Host cells contain complement regulatory proteins that inhibit complement system activation
  - - - Dendritic Cells
    - - NK Cells
- - - - Mature in the bone marrow
        
        A mechanism of negative selection is then used to eliminate self-reacting B cells and minimise the risk of autoimmunity. Negative selection of self-reacting B cells can involve elimination by apoptosis, editing or modification of the receipts so they are no longer self-reactive, or induction of energy in the B cell
      - Form from hematopeietic stem cells
    - - T -cell independent activation of B cells involves cross-linkage of BCR's by repetitive nonprotein antigen epitopes. It is characterised by the production of IgM by plasma cells and does not produce memory of B cells.
    - - B-cell receptors (BCR's) are membrane-bound monomeric forms of IgD and IgM that bind specific antigen epitopes with their Fab antigen-binding regions. Diversity of antigen bidding specificity is created by genetic rearrangement of V, D, and J segments similar to the mechanism used for TCR diversity
    - - T cell-dependent activation of B cells involves: processing and presentation of protein antigens to helper T cells, activation of the B cells by cytokines secreted from activated TH2 cells, and plasma cells that produce different classes of antibodies as a result of class switching. Memory B cells are also produced.
  - - - Macrophages
        
        Once they destroy a microbe they turn into a APC and present it to T-cells
      - Dendritic cells
        
        Found in the peripheral lymphoid organs and the external continuous epithelium
        
        Capture antigens via mannose receptors and soluble antigens are captured via pinocytosis
        
        Initial inducers and most common APC's
      - B -cells
        
        Ingest antigens and present them to T-cells
      - APC's travel through the lymphatic vessels or blood vessels to go to an area with high amounts of T-cells. They are attracted to this area due to the expression of CCR7, which is a surface receptor specific for cytokines from T-cells.
    - - 2 main regions
        
        Variable V
        
        Even within the V regions there are hyper variable areas called complementary determine regions (CDR's) they form the binding area's
        
        Variable C
    - - Found on B and T cells, are used to activate them
      - All antigens are presented on histocompatibility complex (MHC) otherwise it won't be recognised by a T-cell
        
        Class II is used for regular antigen presentation
        
        Activates CD4 T-cells (helper cells)
        
        APC synthesise class II MHC molecules, transport its vesicles. The MHC vesicle merges with the ingested antigen causing them to bind and be presented
        
        Class I MHC is used when a host cell is infected
        
        Activates CD8 T-cells (killer cells)
        
        When a cell starts creating foreign proteins they are broken down into smalle peptides. these peptides can bind to MHC molecules and present them
  - - - MHC class II of APC binds to CD4 receptor
        
        T-killer effector cells
        
        Killing of antigen-expressing cell
        
        perforin, serine, proteases
        
        Apoptosis
    - - MHC Class I of APC binds to CD8 receptor
        
        T-helper effector cell
        
        Th1
        
        Cellular immune response
        
        Help activate macrophages and cytotoxic T-cells
        
        Th2
        
        Humoral immune response
        
        Help activate B-cells
  - - - Primary Immunoglobulins
        
        IgM
        
        Part of the primary response and is the first antibody made; activates the classical pathway of complement
        
        Has 10 antigen bidding sites (Pentamer)
      - Secondary Immunoglobulins
        
        IgA
        
        Can be transported over mucosal epithelium hence it plays a role in mucosal immunity and in neutralisation of microbes and toxins
        
        Has 4 antigen binding sites (Dimer)
        
        IgE
        
        Bind to Fc receptors on Mast cells. involved in the defence of helminths and mast cell degranulation
        
        Has 2 antigen binding sites (Monomer)
        
        IgG
        
        Binds to Fc receptors on macrophages. Neutralises microbes and toxins, opsonisation of antigens for phagocytosis by macrophages and neutrophils. Activates the classical pathway of complement, ensures neonatal immunity by transferring maternal antibody across placenta and gut, feedback inhibit of B-cell activation. Antibody dependent cellular cytotoxicity mediated by NK cells
        
        Has 2 antigen biding sites (Monomer)
    - - 15% IgA
      - 75% IgG
      - 9% IgM
      - 0.2% D
      - 0.004% IgE
    - - 2 light chains
        
        1 variable domain
        
        1 constant domain
      - 2 heavy chains
        
        Constant part is divided into 3 domains in IgG and IgA and 4 parts in IgM and IgE
        
        Same composition as light chains
      - domain is about 110 amino acids long, only 5-10 amino acids are needed in hyper-variable regions for antigen recognition. antigen binds site is the amine site