Immune System Part II PDF

Immune System Part II  Inflammation 1 Inflammation—local defensive response to tissue injury, including trauma and infection General purposes of inflammation Limits spread of pathogens, then destroys them Remov...

Immune System Part II  Inflammation 1 Inflammation—local defensive response to tissue injury, including trauma and infection General purposes of inflammation Limits spread of pathogens, then destroys them Removes debris from damaged tissue Initiates tissue repair Four cardinal signs of inflammation Redness, swelling, heat, pain © McGraw Hill 3 © McGraw Hill 4  Inflammation 2 Suffix -itis denotes inflammation of specific organs: arthritis, pancreatitis, dermatitis Cytokines—small proteins that regulate inflammation and immunity Secreted mainly by leukocytes Alter physiology of receiving cell Act at short range, neighboring cells (paracrines) or the same cell that secretes them (autocrines) Include interferon, interleukins, tumor necrosis factor, chemotactic factors, and others © McGraw Hill 5  Inflammation 3 Three major processes of inflammation: Mobilization of body defenses Containment and destruction of pathogens Tissue cleanup and repair © McGraw Hill 6  Mobilization of Defenses 1 Most immediate requirement after tissue injury is to get defensive leukocytes to the site quickly Achieved by local hyperemia— increasing blood flow Local vasodilation due to vasoactive chemicals Histamine, leukotrienes, and other cytokines Secreted by basophils, mast cells, cells damaged by trauma, toxins, or organisms triggering inflammation Hyperemia also washes toxins and metabolic waste from the site more rapidly © McGraw Hill 7  Mobilization of Defenses 2 Vasoactive chemicals also stimulate endothelial cells to contract, thereby widening gaps between them This increases capillary permeability Fluid, leukocytes, and plasma proteins leave bloodstream Including complement, antibodies, and clotting proteins Selectins: cell-adhesion molecules made by endothelial cells that aid in the recruitment of leukocytes Make membranes sticky, so leukocytes adhere to vessel wall (margination) Diapedesis or emigration: leukocytes crawl through gaps in the endothelial cells and enter tissue fluid Extravasated: cells and chemicals that have left the bloodstream © McGraw Hill 8  Mobilization of Defenses 3 Basis for the four cardinal signs of inflammation Heat: results from hyperemia Redness: due to hyperemia, and extravasated RBCs in the tissue Swelling (edema): due to increased fluid filtration from the capillaries Pain: from direct injury to the nerves, pressure on the nerves from edema, stimulation of pain receptors by prostaglandins, bacterial toxins, and bradykinin © McGraw Hill 9  Mobilization of Defenses 4 Neutrophil behavior Margination Selectins cause leukocytes to adhere to blood vessel walls Diapedesis (emigration) Leukocytes squeeze between endothelial cells into tissue space © McGraw Hill 10  Diapedesis © McGraw Hill 11  Containment and Destruction of Pathogens Priority of inflammation is to prevent pathogens from spreading throughout body Fibrinogen that filters into tissue fluid clots Forms a sticky mesh that walls off microbes Heparin prevents clotting at site of injury Pathogens are in a fluid pocket surrounded by clot Attacked by antibodies, phagocytes, and other defenses © McGraw Hill 12  Containment and Destruction of Pathogens 2 Neutrophils, the chief enemy of bacteria, accumulate at the injury site within an hour After leaving the bloodstream, they exhibit chemotaxis Chemotaxis—attraction to chemicals such as bradykinin and leukotrienes that guide them to the injury site © McGraw Hill 13  Containment and Destruction of Pathogens 3 Neutrophils quickly respond to and kill bacteria Phagocytosis Respiratory burst Secrete cytokines for recruitment of macrophages and additional neutrophils Macrophages and T cells secrete colony-stimulating factor to stimulate leukopoiesis (production of more leukocytes) thereby raising WBC counts in blood Neutrophilia—5,000 cells/μL to 25,000 cells/μL in bacterial infection Eosinophilia—elevated eosinophil count in allergy or parasitic infection © McGraw Hill 14  Tissue Cleanup and Repair 1 Monocytes—the primary agents of tissue cleanup and repair Arrive in 8 to 12 hours and become macrophages Engulf and destroy bacteria, damaged host cells, and dead and dying neutrophils © McGraw Hill 15  Tissue Cleanup and Repair 2 Edema contributes to tissue cleanup Swelling compresses veins and reduces venous drainage Forces open valves of lymphatic capillaries, promoting lymphatic drainage Lymphatics collect and remove bacteria, dead cells, proteins, and tissue debris better than blood capillaries Pus—yellow accumulation of dead neutrophils, bacteria, cellular debris, and tissue fluid Abscess: accumulation of pus in a tissue cavity © McGraw Hill 16 © McGraw Hill 17  Tissue Cleanup and Repair Platelet-derived growth factor is secreted by blood platelets and endothelial cells in injured area Stimulates fibroblasts to multiply Synthesizes collagen Hyperemia delivers oxygen, amino acids, and other necessities for protein synthesis © McGraw Hill 18  Tissue Cleanup and Repair 4 Increased heat increases metabolic rate, speeds mitosis and tissue repair Fibrin clot forms a scaffold for tissue reconstruction Pain makes us limit the use of a body part so it has a chance to rest and heal © McGraw Hill 19 © McGraw Hill 20  General Aspects of Adaptive Immunity Immune system—a large population of widely distributed cells that recognize foreign substances and act to neutralize or destroy them Three characteristics distinguish adaptive immunity from innate immunity Systemic effect: throughout the body Specificity: immunity directed against a particular pathogen Memory: when reexposed to the same pathogen, the body reacts so quickly that there is no noticeable illness © McGraw Hill 21  FORMS OF ADAPTIVE IMMUNITY 1  Two types of adaptive immunity: Cellular (cell-mediated) immunity  Lymphocytes directly attack and destroy foreign cells or diseased host cells  Rids the body of pathogens that reside inside human cells, where they are inaccessible to antibodies  Kills cells that harbor them © McGraw Hill 22  Forms of Adaptive Immunity 2 Two types of adaptive immunity (continued): Humoral (antibody-mediated) immunity Mediated by antibodies that do not directly destroy a pathogen but tag it for destruction Many antibodies are dissolved in body fluids (“humors”) Effective against extracellular viruses, bacteria, yeasts, protozoans, and molecular (noncellular) disease agents such as toxins, venoms, and allergens © McGraw Hill 23  Forms of Immunity 1 Natural active immunity Production of one’s own antibodies or T cells as a result of infection or natural exposure to antigen Artificial active immunity Production of one’s own antibodies or T cells as a result of vaccination against disease Vaccine: consists of dead or attenuated (weakened) pathogens that stimulate the immune response without causing the disease Booster shots: periodic immunizations to stimulate immune memory to maintain a high level of protection © McGraw Hill 24  Forms of Immunity 2 Natural passive immunity Temporary immunity that results from antibodies produced by another person Fetus acquires antibodies from mother through placenta, milk Artificial passive immunity Temporary immunity that results from the injection of immune serum (antibodies) from another person or animal Treatment for snakebite, botulism, rabies, tetanus, and other diseases © McGraw Hill 25  Antigens 1 Antigen—any molecule that triggers an immune response Large molecular weights of over 10,000 amu Complex molecules with structures unique to the individual Proteins, polysaccharides, glycoproteins, glycolipids Characteristics enable body to distinguish “self” molecules from foreign ones © McGraw Hill 26  Antigens 2 Haptens—too small to be antigenic in themselves Can trigger an immune response by combining with a host macromolecule and creating a complex that the body recognizes as foreign Subsequently, haptens alone may trigger response Cosmetics, detergents, industrial chemicals, poison ivy, and animal dander Penicillin binds to host proteins in allergic individuals © McGraw Hill 27 © McGraw Hill 28  Antibody Classes 1 Antibody classes are named for the structure of their C region IgA: monomer in plasma; dimer in mucus, saliva, tears, milk, and intestinal secretions Prevents pathogen adherence to epithelia and penetrating underlying tissues Provides passive immunity to newborns IgD: monomer; B cell transmembrane antigen receptor Thought to function in B cell activation by antigens © McGraw Hill 29  Antibody Classes 2 Antibody classes (continued): IgE: monomer; transmembrane protein on basophils and mast cells Stimulates release of histamine and other chemical mediators of inflammation and allergy Attracts eosinophils to parasitic infections Produces immediate hypersensitivity reactions © McGraw Hill 30  Antibody Classes 3 Antibody classes (continued): IgG: monomer; constitutes 80% of circulating antibodies Crosses placenta to fetus, secreted in secondary immune response, complement fixation IgM: pentamer in plasma and lymph Secreted in primary immune response, agglutination, complement fixation © McGraw Hill 31  Antibody Diversity Human immune system capable of as many as 1 trillion different antibodies But there are as few as 20,000 genes in the human genome, so the variety of proteins must be accomplished by: Somatic recombination DNA segments shuffled and form new combinations of base sequences to produce antibody genes Somatic hypermutation B cells in lymph nodules rapidly mutate creating new sequences © McGraw Hill 32 © McGraw Hill 33