Patho unit 4 Ch.6

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Patho unit 4 Ch.6
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Patho unit 4 Ch.6
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  1. Acquired Immunity
    • Third line of defense:
    •   -Specific
    •    -Responds to a unique pathogen
    •   -Adaptive 
    •    -Variable response
    •   -Two components:
    •    -Cell mediated
    •    -Antibody-mediated ("humoral")- fluids
  2. Lymphocytes
    • Most important cells of the adaptive immune response
    •   -make up only 20-40% of the circulating WBCs, but there are many more in the secondary lymph organs
    • Originate in the bone marrow as lymphocyte precursors or stem cells 
    • They mature either in the bone marrow or in the lymph system
    •   -here the precursor cells will differentiate into functional lymphocytes
    •     -T cells -thymus
    •     -B cells -bone marrow
  3. Lymphatic system
    • Lymphocytes are very specific for certain antigens
    • they must circulate in the lymphatic system to have the highest chance of coming in contact with their antigenic match
    • The success of the immune system hinges on the cooperation and function of both cell-mediated and antibody-mediated (humoral) immunities
  4. B Lymphocytes
    • When stimulated, either directly or indirectly, B lymphocytes develop into plasma cells
    • The proteins released from plasma cells are antibodies
    • This is called antibody-mediated (humoral) immunity
  5. T Lymphocytes
    • Recognizes specific antigens
    • Can directly attack abnormal cells
    • Mediate adaptive immune responses
    • this is called cell-mediated immunity
    •   -T helper
    •   -Tcytotoxic
    •   -T memory
    •   -T regulator
  6. Immunogen
    A molecule that will induce (stimulate) an immune response
  7. Antigen
    • Molecule or molecular fragment that bind with products of the immune system (antibodies, T-cells, B-cells)
    •   -Identifies the cell as self or non-self
    •   -identifies the type of cell
    •   -Ex: Viruses, bacteria, fungi, parasites, pollens, foods, drugs, cell markers, tumor cell markers
  8. A molecule or molecular fragment is more immunogenic/ antigenic if it is :
    • Large in size
    •   -100 amino acids in a small protein
    • Organic
    • Complex in structure
    • Foreign, "non-self", or at least recognized as non-self
  9. Haptens
    • a molecule that is not large enough to react with the immune response by itself
    • It may trigger an immune response when bound to a larger molecule
    •   -Medications may act as haptens if they bind to something like a RBC surface protein and it could then become immunogenic
  10. Allergen
    an antigen that induces an allergic response
  11. Epitopes= Antigenic Determinants
    • If and antigen is large and complex enough, there can be multiple immunogenic portions of the antigen
    •   -if a patient has acute hepatitis B, they produce at least three different antibodies to the virus
  12. Acquired Adaptive Immunity
    • Natural immunity: immunity not gained through modern medicine
    • Artificial immunity: gained through artificial means
    • Active immunity: The body responds to a pathogen (antigen) to make antibodies (long-term immunity)
    • Passive immunity: (Mom and Baby) the body simply receives antibodies with no effort of its own. (short-term immunity)
  13. Examples of Acquired Adaptive immunity
    • Natural Active: Hepatitis A stimulates the production of anti-hepatitis A antibodies
    • Natural Passive: a baby receives antibodies from its mother through the placenta and breast milk
    • Artificial Active: a person receives an injection of an attenuated (changed/weakened) pathogen that stimulates the body to form an antibody
    • Artificial Passive: injection of prepared antibody
  14. Antigen and Antibody
    • The adaptive immune system responds to antigens
    • One of the results of this is production of of and antibody
    • And antibody is a protein molecule that can bind strongly to and antigen
    •   -binding is so strong, its almost covalent (ie permanent)
    •   -antibodies are made in billions of different forms to bind any molecule the immune system may encounter
  15. Immunoglobulins (Antibodies)
    • known as : gamma globulins, immunoglobulins, and antibodies
    • Ig are distinguished by structure, location, and function
    •   -Classes: IgM, IgG, IgA, IgE, IgD
  16. Immunoglobulin Structure
    • Fab (fragment antigen binding) fragment- the portion of the antibody that binds to the antigen
    • Fc (fragment crystalline) fragment- portion of the the antibody that remains constant
    • Base unit (monomer) structure- 2 heavy chains and 2 light chains
  17. IgM
    • 10% of total plasma antibody
    • Pentamer
    • 10 heavy and 10 light chains
    • Very effective activator of the complement system
  18. IgG
    • 75% of plasma antibody
    • Monomer
    • Actively transported across the placenta (maternal-fetal)
    • Longest half-life of the immunoglobulins
    •   -Long-term immunity
  19. IgA
    • present in plasma and body secretionscontains
    • sIgA- secretory component
    •   - protects from enzymatic destruction
    • Lacrimal glands, salivary glands, and lymphoid tissues in the breasts, bronchi, intestines, and GI tract
    • Protects against pathogens that are inhaled, swallowed, or come in contact with external surfaces.
  20. Secretory immune system
    • IgA secreted in gut by mucosal-associated lymphoid tissue (MALT)
    • These are similar to lymph nodes, but protrude into gut lumen 
    • M cells found in Peyer's patches within gut wall pass antigens from lumen tothe MALT beneath
    • There, B cells are stimulated to make IgAs
    • Other epithelial surfaces use a similar system
  21. IgE
    • Low plasma concentration
    • Bound to eosinophils, basophils and mast cells
    • Triggers release of histamine from mast cells
  22. Primary vs Secondary Immune Responses
    • When stimulated initially, plasma cells begin making large amounts of antibody
    • 1. IgMs first -binds more antigen
    • 2. IgGs later
    • Memory B cells stay in a resting state until there is a secondary exposure of the antigen
    • the whole process of presentation is made faster because the immune system has developed memory
  23. Fetal and Neonatal Immunity
    • Innate immunity is functioning (at reduced capacity) at birth
    •   -about half of newborns have rash (erythema toxicum neonatorium) as flora colonize skin, causing inflammation
    •   -IgG crosses the blood-placenta barrier
    •     -At birth babies IgG levels are in equilibrium with mothers so baby has a natural passive immunity
    •     -Baby produces no IgG of his own at birth
    •   IgM dose not cross the blood-placenta barrier
    •     -Must be made by newborn
    •     -Newborn levels 20% those of adult, and it takes about 2 years to reach adult levels
    • IgA levels very low at birth
    •     -Adult values of salivary IgA reached at about 2 month
    •     -Mothers breast milk provides passive natural immunity, via her secreted IgA
  24. Major Histocompatibility Complex (MHC Molecule and Human Leukocyte Antigens)
    • A group of genes on chromosome 6
    • MHC genes code for MHC proteins
    • The MHC genes are grouped in classes (classI,II, and III)
    • Because of their role in tissue transplants, the MHC molecules are also referred to as human leukocyte antigen (HLA)
    •   -A person has a blood type, and they also have an HLA type
  25. Surface cell Markers of Immune cells
    Major Histocompatibility Complex
    (Human Leukocyte Antigens)
    • MHC molecules are the flags that identify cells
    •   -who they belong to 
    •   -what organ/tissue they belong to
    • MHC molecules provide information about what the cell has encountered 
    •   what the antigen-presenting cell ate
    •    -Exogenous antigen
    •   Whether a cell is infected with a virus
    •    -Endogenous antigen
  26. MHC (HLA) classI
    • molecules are located on all nucleated cells
    •   -Present endogenous antigen
  27. MHC (HLA) class II
    • Molecules are located on professional antigen presenting cells (APCs)
    •   -Macrophages, dendritic cells, and B lymphocytes 
    •   - Present Exogenous Antigen
  28. Cell Surface Markers
    • Clusters of Differentiation (CD) is another protocol for identification of cell surface markers
    •   -They are not on a particular chromosome
    •   Over 300 have been Identified 
    • Ex:
    •   -all Leukocyte groups = CD45+
    •   -Granulocyte =  CD45+, CD15+
    •   -monocyte = CD45+, CD14+
    •   -T lymphocyte =  CD45+, CD3+
    •   -T helper cell =  CD45+, CD3+, CD4+
    •   -T cytotoxic cell =  CD45+, CD3+, CD8+
    •   -B lymphocyte =  CD45+, CD19+
  29. Links between the innate and adaptive Immune systems
    • Innate immune system
    •   -Neutrophils
    •   -Monocytes/Macrophages
    • Linking innate and adaptive immune systems 
    •   -Antigen-Presenting Cells (APCs)
    •    -Macrophage
    •    -Dentritic cells
    •    -Some B cells
    • Adaptive immune system
    •   -T cells (cell-mediated immunity)
    •   -B cells (antibody-mediated immunity)
    •   -Both B and T cells produce memory cells to speed responses
  30. Thelper cells (CD4+)
    • They are recruited by advertising of antigens displayed on the APC
    • When they see the antigen, they release cytokines and stimulate cell division by autocrine activation
    • As they divide they form: 
    •   -T-memory cells- speed future response 
    •   -T-helper1 cells- cell mediated immunity 
    •   -T-helper2 cells- activate antibody-mediated immunity
  31. Tcytotoxic cells (CD8+)
    • Activated by Thelper lymphocytes 
    • When activated, release compounds that kill cancerous or virally infected cells
    • Apoptosis is preferred for virally infected cells    
    •   -DNA fragmentation reduces risk of virus re-infection
    • Perforin used to trigger cytolysis
  32. True or false
    Infected cells that display viral antigens on their membranes are destroyed by cytotoxic T cells
    True
  33. T regulator (T suppressor) Cells
    • Little known about these cells 
    •   Lack identified CD marker, making them harder to study
    • seems to down-regulate immune response and save normal cells from destruction
    • Over-active T reg cells --cancer can get the upper hand (lowers immune surveillance)
    • Under-active T reg cells --autoimmune disease (lowers protection of normal cells)

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