Chapter 21: The Immune System Flashcards
Immunity:
o The Immune system battles disease. o The Immune system has two intrinsic systems: o Nonspecific (innate) defense system. o Specific (adaptive) defense system. o Nonspecific or Innate defense system has two lines of defense o First line of defense is external body membranes (skin and mucosae) o Second line of defense is internal body defenses: antimicrobial proteins, antimicrobial cells, fever, and the inflammatory process.
Characteristics of Innate Defenses:
o Present at birth.
o Act instantly or very quickly.
o No prior exposure necessary.
o Response is the same EACH TIME the body is exposed to any foreign thing.
o Responses are effective against a wide range of pathogen (even pathogens) our body has never seen before.
o Works with the specific defense mechanisms.
Innate Defenses (1st Line Defense):
o First line of defense = Surface barriers
o Skin & mucous membranes, and their secretions
o Physical barrier to most microorganisms
o Keratin is resistant to weak acids and bases, bacterial enzymes, and toxins
o Mucosae provide similar mechanical barriers through mucus (mucus cells)
o Protective chemicals inhibit or destroy microorganisms:
o Skin dryness and acidity (lactic acid).
o Lipids in sebum and dermcidin in sweat.
o HCl and protein-digesting enzymes of stomach mucosae.
o Lysozymes from sweat, tears, mucus, and saliva.
o Mucus (from mucous membranes) = sticky trap + lysozymes.
o Respiratory system modifications:
o Mucus-coated hairs in the nose.
o Cilia of upper respiratory tract sweep dust- and bacteria-laden mucus from lower respiratory passages.
o Coughing, sneezing.
o Cerumen.
Innate Defenses (2nd Line Defense):
o Necessary if microorganisms invade deeper tissues:
o Phagocytes (like neutrophils).
o Natural killer (NK) cells (have defensins).
o Inflammatory response (macrophages = come from monocytes; mast cells; WBCs, and inflammatory chemicals).
o Neutrophils, eosinophils, basophils = phagocytes.
o Antimicrobial proteins (interferons and complement proteins).
o Fever.
o Macrophages develop from monocytes to become the chief phagocytic cells:
o Free macrophages wander through tissue space.
o Fixed macrophages are permanent residents of some organs. e.g., Kupffer cells (liver) and microglia (brain).
o Neutrophils = PMNs:
o Become phagocytic on encountering infectious material in tissues (poke holes = defensins).
Mechanisms of Phagocytosis:
o Step 1: Adherence of phagocyte to pathogen
o Facilitated by opsonization, coating of the pathogen by complement proteins made in liver (in other words pathogens are tagged on plasma membranes or marked for destruction).
o Destruction of pathogens once they are “gobbled up” by macrophages.
o Acidification and digestion by lysosomal enzymes.
o Respiratory burst from macrophages:
o Release of cell-killing free radicals and hydrogen peroxide (oxidizing chemicals).
o Activation of additional enzymes.
o Defensins: (in neutrophils) that poke holes in membranes of pathogens.
Events of Phagocytosis:
o 1) Phagocyte adheres to pathogens or debrins.
o 2) Phagocyte forms pseudopods that eventually engulf the particles forming a phagosome.
o 3) Lysosome fuses with the phagocytic vesicle, forming a phagolysosome.
o 4) Lysosomal enzymes digest the particles, leaving a residual body.
o 5) Exocytosis of the vesicle removes indigestible and residual material.
Natural Killer Cells:
o Large granular lymphocytes.
o Induce lysis or apoptosis in cancer cells (tumors) and virus-infected cells by releasing cytoplasmic granules.
o Secrete potent chemicals that enhance the inflammatory response.
Innate (Inflammatory Response):
o The inflammatory response is the LOCAL defensive response of tissue damage.
o Common response to most disease states.
o Purpose of Inflammation:
o Dispose of pathogens and dead cells/debris.
o Prevent spread of infection.
o Prepare the site for tissue repair.
o Cardinal signs of acute inflammation:
o Redness (erythemia or hyperemia = arteriole vasodialation for increased blood flow to area).
o Heat (BV vasodialation causes localized hyperthemia mast cells release histamine and heparin = heat speeds up localized metabolism.
o Swelling (edema caused by increased capillary permeability) = exudate.
o Pain.
o Functions of the surge of exudate from edema:
o Moves foreign material and pushes “bad stuff” into lymphatic vessels.
o Delivers clotting proteins to form a scaffold for repair and to isolate the area.
Phagocyte Mobilization:
o 1) Leukocytosis: release of macrophages and neutrophils (first to the scene!!) from bone marrow in response to leukocytosis-inducing factors from injured cells.
o 2) Margination: neutrophils cling to the walls of capillaries in the inflamed area.
o 3) Diapedesis of neutrophils (movement through tissues and “squeezes” through blood capillaries).
o 4) Chemotaxis: inflammatory chemicals (chemotactic agent) promote positive chemotaxis of neutrophils.
Innate Antimicrobial Proteins (Interferons):
o Interferons (IFNs) and complement proteins:
o Attack microorganisms directly
o Hinder microorganisms’ ability to reproduce
o Small proteins that provide protection against viruses
o Interferons are secreted by the cells of the body that have become infected by a virus, pathogens, bacteria, tumor cells.
o These infected body cells secrete interferons into the IF (interstitial fluid) and they bind to receptors on neighboring cell membranes.
o Neighboring cells receive the signal and make ant-viral substances.
o Interferons also activate macrophages and NK cells.
o Produced by a variety of body cells:
o Lymphocytes produce gamma (γ), or immune, interferon.
o Most other WBCs produce alpha (α) interferon.
o Fibroblasts produce beta (β) interferon.
o Interferons also activate macrophages and mobilize natural killer cells (NKs).
Complement (antimicrobial) Proteins:
o The complement system = 25 blood proteins that circulate in an inactive state (made in liver)
o “Complements” the antibody/antigen reaction
o Major mechanism for destroying foreign substances when activated
o When activated, 3 important effects:
o Inflammaton (enhances the inflammatory response = chemotaxis, histamine release)
o Enhanced Phagocytosis via opsonization.
o Cytolysis via production of membrane attack complexes = MACS which pokes holes in the membranes of micoorganisms.
-Innate= Fever:
o Systemic response to invading microorganisms.
o Abnormal elevation of body temperature.
o Neutrophils and macrophages exposed to foreign substances secrete pyrogens.
o Pyrogens reset the body’s thermostat upward = hypothalamus.
o High fevers are dangerous because heat denatures enzymes.
o Benefits of moderate fever =intensifies the effects of interferons, enhances phagocytosis, sequesters liver and spleen in releasing iron, zinc, copper which is needed for bacterial replication, elevates metabolic rate and hence tissue repair.
Special Immunity:
o Different from innate (non-specific) immunity because it is:
o 1) Systemic = not restricted to the initial site of infection.
o 2) Specific = fights a very specific pathogen or part of a pathogen.
o 3) Has memory = when the body is exposed a second time to the same pathogen, the specific immune system responds more quickly and more forcefully = T & B cells that become memory cells.
o 4) Depends heavily on lymphocytes = T cells / B cells.
Two Major Forms of Specific Immunity:
o 1) Humoral (antibody-mediated) immunity: B-lymphocytes differentiate into plasma cells = secretes antibodies.
o 2) Cellular (cell-mediated) immunity: T-lymphoctyes directly attack foreign cells or diseased host cells.
Other Classifications of Specific Immunity:
o Active Immunity: Your body makes its own antibodies or activates its own T-cells against the pathogen. Natural (natural exposure to an antigen). Artificial (exposure via vaccination).
o Passive Immunity: Your body acquires antibodies or T-cells from another person or an animal. Natural = antibodies, T-cells to fetus via placenta and newborn via breast milk. Artificial = injection of immune serum (already has antibodies and T-cells) from another animal or person.
