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Concept map 1 - Coggle Diagram

- - - - strongest barrier to infection
      - comprised of cells...
        
        dead
        
        tightly packed
        
        keratinized
        
        waterproofing
    - - urogenital tract
        
        uterus
        
        bladder
        
        vagina
      - gastrointestinal tract
        
        oral cavity
        
        esophagus
        
        stomach
        
        pancreas
        
        intestine
      - respiratory tract
        
        sinus
        
        trachea
        
        lungs
  - - - phagocytosis
        
        lysosome
        
        pH change
        
        enzymes (e.g. lysozyme)
        
        toxic radicals
        
        drawbacks
        
        survive/disguised by phagocytes
        
        Mycobacterium tuberculosis (bacteria)
        
        HIV (virus)
        
        Chlamydia (bacteria)
        
        Plasmodium (protozoa)
        
        fatally sensitive to some microbes: toxins/enzymes that require low pH of lysosome
        
        Bacillus anthracis (bacteria)
    - - complement proteins
      - constantly produced by liver
      - circulate in blood
      - C1-C9
        
        constantly made by liver
        
        circulate in blood
        
        3 pathways for activation
        
        alternative pathway
        
        complement activated directly by binding pathogen
        
        C3 reacts with H2O and forms iC3
        
        pathogen surfaces promote this due to charges
        
        factor B binds to iC3
        
        factor D cleaves factor B when factor B when factor B is bound to iC3 (or C3b)
        
        Ba fragment is soluble
        
        Bb fragment remains bound to iC3 generating iC3Bb
        
        iC3b is a protease that cleaves other C3 molecules
        
        generates C3a and C3b
        
        complement fixation of C3b causes cascade
        
        lectin pathway
        
        requires antibody binding pathogen
        
        classical pathway
        
        requires antibody binding pathogen
        
        C3
        
        essential for for all pathways
        
        contains a high-energy thioester bond buried within the protein
        
        upon activation, C3 protein is cleaved into C3a and C3b
        
        C3a is a soluble protein that acts as a cytokine
        
        C3b contains the now-exposed high-energy thioester bond
        
        C3b either bonds to water or covalently bonds to pathogen surface to act as a beacon
        
        complement fixation is the attachment of C3b to pathogen
        
        outcomes
        
        Roles of C3a and C5a
        
        C3a and C5a bind receptors on mast cells and basophils
        
        mast cells and basophils initiateinflammation
        
        excessive C3a or C5a results in systemic inflammation
        
        leads to anaphylactic shock
        
        C3a and C5a are also called anaphylatoxins
        
        C5a is more potent
        
        more stable
      - membrane attack complex
        
        punches holes in pathogen cell membrane
        
        can be activated by any complement
        
        formation of MAC
        
        C3b2Bb forms when C3bBb binds C3b
        
        C5 is cut by C3b2Bb
        
        now have C5a and C5b
        
        C5a is soluble
        
        C6 stabilizes C5b
        
        makes C5b6
        
        C7 binds C5b67
        
        now have C5b67
        
        C8 binds C5b67 and inserts into membrane
        
        now have C5b678
        
        C9 binds and polymerizes to form MAC
        
        MAC regulation
        
        recognizing 'self' cells
        
        Homologous Restriction Factor (HRF) and CD59
        
        prevent C9 recruitment
    - - redness
      - pain
      - heat
      - edema
      - purposes
        
        destroy microbes/toxins infecting area
        
        confine the microbe/products
        
        repair tissue damage
      - results from injury to tissue and macrophage cytokine production
      - steps of inflammation
        
        step 1: injury/infection activates effector cells to release cytokines(messenger molecules)
        
        step 2: increased blood vessel permeability and vasodilation allowing leakage of blood into tissue causing redness, edema, and heat
        
        step 3: phagocyte migration causing pain to target immune cells to infection
        
        step 4: tissue repair (starts immediately after infection and does not complete until after infection is cleared
- - - - T cell precursors originate from bone marrow
  - - - tonsils
      - adenoids
      - appendix
      - peyer's patches
        
        gut lumen
        
        epithelium
        
        M cell
        
        dendritic cell
        
        follicle
        
        B cells
        
        T cells
        
        efferent lymphatics
        
        germinal center
  - - - proliferating, active B cells with some T cells, macrophages, and follicular dendritic cells
    - - active T cells can move to follicles
- - - - antibody producing/plasma (B) cells
      - memory cells (B or T)
    - - lymphocytes with protein receptors that recognize pathogen are chosen
    - - selected lymphocytes multiply
- - - - erythroid
      - myeloid
        
        neutrophils
        
        circulate in bloodstream
        
        phagocytes
        
        eosinophils
        
        circulate in blood stream
        
        parasite removal
        
        basophils
        
        histamine, parasites
        
        circulate in blood stream
        
        monocytes
        
        circulate in bloodstream
        
        mature into macrophages
        
        phagocytes
        
        macrophages
        
        sedentary tissue cells
        
        phagocytosis
        
        macrophages and complement system
        
        complement receptor 1 (CR1)
        
        protein receptor on macrophages
        
        binds C3b
        
        allows macrophage to better recognize and engulf marked bacteria
        
        dendritic cells
        
        tissue localized until activated
        
        initiate adaptive response
        
        mast cells
        
        connective tissue cells
        
        contrinute to inflammation
        
        histamine
      - lymphoid
        
        natural killer cells
        
        destroy infected or mutated 'self' cells by apoptosis
        
        T lymphocytes
        
        cell mediated immunity
        
        T cells are also known as T lymphocytes
        
        T cells circulate in immature form until activated (clonal selection)
        
        naive T cells develop into...
        
        helper T cell
        
        regulatory T cell
        
        memory T cell
        
        cytotoxic T cell
        
        B lymphocytes
        
        humoral immunity
        
        B cells are also known as B lymphocytes
        
        immature B cells have cell surface receptors and circulate
        
        Plasma cells: mature B cells that secrete antibodies
        
        ANTIBODIES
        
        neutralization of pathogen/toxin via binding/preventing host attachment
        
        opsonization (coating) of pathogen to promote phagocytosis
        
        2 more items...
        
        antibody-dependent cell-mediated cytotoxicity (ADCC) activates natural killer cells
  - - - antigen receptors
      - variable region different on every circulating T cell
    - - surface immunoglobulins
      - variable region different on ever B cell receptor or secreted antibody