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Chapter 021

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  • The immune system protects the body from pathogens and other foreign agents, including pollens, toxins, and the body’s cells that have gone astray (cancer cells).
    The slide’s illustration shows specific and nonspecific immunity.
  • The first line of defense includes mechanical barriers (intact skin and mucous membrane), chemical barriers (gastric juice and tears), and reflexes (sneezing and vomiting).
    Why do health care professionals wear gloves while handling patients; secretions?
    Gloves maintain the body’s first line of defense against infection by preventing pathogens from entering the body.
  • The first line of defense (barriers and reflexes) is shown in the top row of the figure.
    The second line of defense is shown in the lower row of the figure and will be discussed in the following five slides.
  • Phagocytosis involves the ingestion of pathogens and tissue debris by white blood cells. The neutrophils and monocytes are motile, and other phagocytes are fixed within a particular tissue.
    The phagocytic WBCs must go to the site of infection by following a chemical trail to it. The cartoon showing the bloodhound illustrates the processes of diapedesis (squeezing through gaps in the capillary walls) and chemotaxis (picking up the “scent” of the infected cell).
    In phagocytosis, the WBC engulfs the pathogen and chemicals within the WBC destroy it.
    Vigorous phagocytosis can cause pus and abscess formation.
  • Blood flow increases to an injured area, causing redness and heat.
    Injured tissue leaks fluid into interstitial space causing swelling, which presses on nerve endings to cause pain.
    In addition to infection, what are some causes of inflammation?
    Causes of inflammation include contact with irritants such as poison ivy, friction rub, radiation, and some diseases such as arthritis.
  • Most pathogens are “happy” at normal temperature, so an elevated temperature helps fight infection.
    A fever results from the body resetting its internal thermostat (hypothalamus). Hyperthermia (e.g., a baby left in a hot car) results from the body’s inability to lose heat rather than a resetting of the thermostat. Therefore, a fever is treated with aspirin, but hyperthermia does not respond to aspirin.
    Very high fevers must be reduced so they do not cause febrile seizures and brain damage, but generally fever helps the body fight infection.
  • Cells infected with virus produce interferons, which then protect surrounding cells from viral infection.
    In their inactive form, complement proteins circulate in the blood. When activated, they swarm bacteria, making them more vulnerable to phagocytosis by leukocytes.
  • Natural killer cells are lymphocytes that act nonspecifically.
    They also engage in phagocytosis.
  • T cells and B cells are lymphocytes and engage in specific immunity. T cells comprise 70% to 80% of the blood’s lymphocytes.
    The T cells engage in cell-mediated immunity; they attack pathogens directly by punching holes in the cell membrane and secreting lymphokines. The lymphokines enhance phagocytosis.
    The B cells engage in antibody-mediated immunity. The activated B cells secrete antibodies, which engage in an antigen-antibody reaction within the pathogen. The resulting agglutination or clumping destroys the pathogen.
    Macrophages help activate T and B cells.
  • A macrophage ingests an antigen and pushes it to its surface. This is called “antigen presentation” and activates T cells.
    The activation of the T cell produces a clone with four types of cells.
    Killer T cells engage in cell-to-cell combat.
    Helper T cells stimulate further T-cell and B-cell activation.
    Suppressor T cells inhibit the immune response when the antigen has been destroyed.
    Memory T cells do not participate in cell-mediated combat. They remember initial infection and, if the antigen is presented a second time, the memory T cells reproduce to allow a faster immune response.
  • The activated B cell produces a clone with two types of cells.
    Plasma cells secrete antibodies that are specific to the antigen that caused their activation. The antibodies attack the antigen.
    The memory B cells remember the antigen and, if it is presented again, they produce a rush of antibodies.
    In a person with HIV, the virus interferes with the production of helper T cells, which activate both T cells and B cells.
  • There are four abundant immunoglobulins (antibodies).
    IgG, found in plasma and body fluids, is particularly effective against bacteria, viruses, and toxins.
    IgA is found primarily in breast milk, tears, and gastric juices and helps protect against infection.
    IgM, found in plasma, is associated with blood type compatibility or incompatibility.
    IgE is involved in an immediate hypersensitivity reaction and will be described in the discussion of anaphylaxis.
  • The initial response to an antigen is called the primary response. The primary response is associated with a low plasma level of antibodies and slow development of antibodies.
    The secondary response, however, is a quick response and involves a larger number of antibodies, thanks to the activated memory cells.
    This figure illustrates the primary and secondary responses to an antigen.
    A first exposure to the measles typically produces the signs and symptoms of the disease, but a second exposure does not. Why?
    The memory cells “remember” the initial exposure to the measles antigen and cause the plasma cells to quickly secrete a lot of measles antibodies.
  • Immunity can be acquired naturally: by getting a disease or by getting antibodies across the placenta or in breast milk.
    Immunity can also be acquired artificiallyfor example, by getting a vaccine or immune globulin.
    All these methods of acquiring immunity will be developed in future slides.
  • When you get a disease and make antibodies against it, the process is called active immunity because you made the antibodies. Active immunity is considered long-lasting.
    When you receive antibodies from your mother, your mother made the antibodies, so the process is called passive immunity. This type of immunity is short-acting, because your body eventually destroys those antibodies.
    Why does breast-feeding give babies an immunological advantage?
    The breast milk constantly transfers the mother’s antibodies to the baby.
  • A vaccine contains an attenuated or weakened form of the pathogen or a piece of the pathogen’s cell membrane. Because it stimulates the production of antibodies in the recipient, it produces active and long-lasting immunity.
    A toxoid produces active immunity in response to a pathogen’s toxin. Immune globulin, antivenoms, and antitoxins confer passive immunity; the human recipient does not make the antibodies.
    For example, measles vaccine produces active immunity against measles and tetanus antitoxin provides passive immunity against tetanus.
  • Treatments for a delayed-onset reaction are removal of the irritant and use of antihistamines and possibly steroids.
    Persons should avoid repeated exposure because the reaction can then develop more quickly and in a more severe form.
  • Step 5, as shown in the illustration, can cause severe systemic effects, including massive vasodilation, a sharp drop in blood pressure and shock, and severe bronchoconstriction. This severe form of the immediate hypersensitivity reaction is called anaphylaxis or anaphylactic shock.
    The treatment for anaphylaxis includes opening the airway and elevating the blood pressure.
  • Some examples of autoimmune disease include thyroiditis, myasthenia gravis, rheumatic fever, rheumatoid arthritis, and some forms of diabetes mellitus.
    Persons who receive organ transplants must be on immunosuppressant drugs such as cyclosporine for the rest of their lives to prevent an attack on the donated organ.
  • Transcript

    • 1. The Human Body in Health and Illness, 4th edition Barbara Herlihy Chapter 21: Immune System 1
    • 2. Lesson 21-1 Objectives • Differentiate between specific and nonspecific immunity. • Describe the process of phagocytosis. • Explain the causes of the signs of inflammation. • Explain the role of fever in fighting infection. • Explain the role of T cells in cell-mediated immunity. Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 2
    • 3. Lesson 21-1 Objectives (cont’d.) • Explain the role of B cells in antibodymediated immunity. • Differentiate between genetic immunity and acquired immunity. • Describe naturally and artificially acquired active and passive immunity. • Identify the steps in the development of anaphylaxis. Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 3
    • 4. Immune System: Classification • Specific immunity protects against one substance. • Nonspecific immunity protects against many substances. Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 4
    • 5. Immunity: Lines of Defense • Nonspecific immunity – First line: Mechanical or chemical barriers, reflexes – Second line: Phagocytosis, inflammation, fever, protective proteins, natural killer cells • Specific immunity – Third line: B and T lymphocytes or B and T cells Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 5
    • 6. Nonspecific Immunity: Lines of Defense Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 6
    • 7. Second Line of Defense: Phagocytosis • Leukocytes go to site of infection. – Diapedesis – Chemotaxis • Leukocytes “eat” – Pathogens – Cellular debris Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 7
    • 8. Second Line of Defense: Inflammation • Classic signs – Redness – Heat – Swelling – Pain Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 8
    • 9. Second Line of Defense: Fever (Pyrexia) • Phagocytosis releases pyrogens. • Pyrogens reset body thermostat upward. • Body temperature rises. • Antipyretics can lower temperature. Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 9
    • 10. Second Line of Defense: Protective Proteins • Interferons are secreted by cells infected by a virus. • Interferons protect other cells from viral replication. • Complement proteins assist WBCs. Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 10
    • 11. Second Line of Defense: NK Cells • A lymphocyte that acts nonspecifically • Effective against many microbes and certain cancer cells Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 11
    • 12. Specific Immunity: 3rd Line of Defense • T cells – Cell-mediated immunity • B cells – Antibody-mediated immunity • Macrophages – Help activate T and B cells Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 12
    • 13. T-Cell Activation • Macrophage ingests antigen • Antigen presentation • Clone produced – Killer T cells – Helper T cells – Suppressor T cells – Memory T cells Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 13
    • 14. B-Cell Activation • Macrophage ingests antigen • Antigen presentation • B cells and helper T cells activated • Clone formed – Plasma cells – Memory B cells Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 14
    • 15. Antigen, Antibody, Immunoglobulin • Antigen: Stimulates formation of antibodies • Antibody: Secreted by B cells, also called immunoglobulins • Antigen-antibody interaction agglutination • Important immunoglobulins – Immunoglobulin G (IgG) – Immunoglobulin A (IgA) – Immunoglobulin M (IgM) – Immunoglobulin E (IgE) Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 15
    • 16. Why is Secondary Response Stronger than Primary Response? Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 16
    • 17. Types of Immunity • Genetic: Inborn and speciesspecific • Acquired: How do you get it? – Naturally – Artificially Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 17
    • 18. Naturally Acquired Immunity • Active: You are exposed to the antigen and you produce antibodies. – Exposure to a virus • Passive: Someone else makes antibodies. – From mother Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 18
    • 19. Artificially Acquired Immunity • Active – Vaccines – Toxoids • Passive – Immune globulin (antibodies made by others) – Antitoxins, antivenoms Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 19
    • 20. Allergic Reaction: Delayed • Occurs in about 48 hours • Usual cause is repeated exposure of skin to irritants (household detergents, poison ivy) • Activates T cells, causing skin eruptions and inflammation (contact dermatitis) Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 20
    • 21. Immediate Hypersensitivity Reaction: Anaphylaxis IgE • Bee venom • IgE binds to mast cells. • Second sting: Venom binds to IgE on mast cell. • Mast cells release histamine. • Histamine drops BP and impairs breathing. Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 21
    • 22. Other Immunological Responses • Autoimmune diseases: Develop in response to self-attack, or autoimmunity • Organ rejection: Recipient’s immune system recognizes donated organ as foreign, mounts immune attack against it Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. 22

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