Resistance of the Body to Infection - Immunity and Allergy (PHYSIO LC6)

Table 1. Difference of the Innate and Acquired Immunity. OUTLINE Innate...

Table 1. Difference of the Innate and Acquired Immunity. OUTLINE Innate Acquired I. IMMUNITY Present at birth Stimulated by antigens A. Acquired Immunity B. Innate Immunity Responds rapidly Slow to start II. ACQUIRED (ADAPTIVE) IMMUNITY A. Immunization Mounts to the same response to all Highly specific B. Basic Types of Acquired Immunity antigens 1. Humoral Immunity No immunologic memory Has immunologic memory 2. Mediated Immunity C. Antigens D. Lymphocytes E. Mechanism for Activating Lymphocyte Clones II. ACQUIRED (ADAPTIVE) IMMUNITY F. Cell-Mediated Immunity G. Humoral Immunity and Antibodies ACQUIRED (ADAPTIVE) IMMUNITY H. Major Histocompatibility Complex Proteins is caused by a special immune system that forms antibodies and/or I. Immunization by Injection of Antigens activated lymphocytes that attack and destroy the specific invading J. Passive Immunity organism or toxin. III. ALLERGY can often bestow an extreme degree of protection. A. Allergy Caused by Activated T-Cells B. Atopic Allergies Associated with Excess IgE Antibodies A. IMMUNIZATION 1. Anaphylaxis Acquired immunity can often bestow an extreme degree of 2. Urticaria protection. For example, certain toxins, such as the paralytic 3. Hay Fever botulinum toxin or the tetanizing toxin of tetanus, can be protected 4. Asthma against in doses as high as 100,000 times the amount that would be lethal without immunity. It is for this reason that the treatment process known as immunization is so important in protecting people against disease and against toxins I. IMMUNITY B. BASIC TYPES OF ACQUIRED IMMUNITY 1. HUMORAL IMMUNITY OR B-CELL IMMUNITY IMMUNITY develops circulating antibodies, which are globulin molecules in the ability to resist almost all types of organisms or toxins that tend the blood plasma capable of attacking the invading agent to damage the tissues and organs of the human body. B lymphocytes produce the antibodies 2. CELL-MEDIATED IMMUNITY OR T-CELL IMMUNITY ACQUIRED IMMUNITY formation of large numbers of activated T lymphocytes, which are Also known as adaptive, and specific immunity specifically crafted in the lymph nodes to destroy the foreign Does not develop until after the body is first attacked by a bacterium, agent virus, or toxin; often, weeks or months are required for the immunity the activated lymphocytes are T lymphocytes to develop. Both the antibodies and activated lymphocytes are formed in the INNATE IMMUNITY lymphoid tissues of the body. Also known as natural, inborn, and nonspecific immunity Immunity that results from general processes, rather than from C. ANTIGENS processes directed at specific disease organisms. Antibody Generators Includes the following aspects: these are proteins or large polysaccharides that initiate the acquired 1. Phagocytosis of bacteria and other invaders by white immunity blood cells and cells of the tissue macrophage system it usually must have a high molecular weight of 8000 or more 2. Destruction of swallowed organisms by the acid the process of antigenicity usually depends on regularly recurring secretions of the stomach and the digestive enzymes molecular groups, called epitopes, on the surface of the large 3. Resistance of the skin to invasion by organisms molecule 4. Presence in the blood of certain chemicals and cells that This factor also explains why proteins and large polysaccharides are attach to foreign organisms or toxins and destroy them. almost always antigenic because both these substances have this Some of these are: stereochemical characteristic a. Lysozyme, a mucolytic polysaccharide that attacks bacteria and causes them to dissolute; b. Basic Polypeptides, which react with and inactivate certain types of gram-positive bacteria; c. The Complement Complex, a system of about 20 proteins that can be activated in various ways to destroy bacteria; d. Natural Killer Lymphocytes that can recognize and destroy foreign cells, tumor cells, and even some infected cells. Figure 1. Antigen-Antibody complex Page 1 of 9 [PHYSIO] 1.06 RESISTANCE OF THE BODY TO INFECTION: Immunity and Allergy – Dr. Kristen Benedict B. Figuerres D. LYMPHOCYTES Found in: Lymph nodes Spleen Submucosal areas of the gastrointestinal tract Thymus Bone marrow Lymphoid tissue ○ The lymphoid tissue is distributed advantageously in the body to intercept invading organisms or toxins before Figure 4. Appearance of the thymus as age progresses. they can spread too widely. T LYMPHOCYTES Gut → Lymphoid tissue of the GI walls They react only against antigens from an outside source, such as Upper respiratory tract → Lymphoid tissue of the throat and from a bacterium, toxin, or even transplanted tissue from another pharynx (including the tonsils and adenoids) person. Peripheral tissues of the body → Lymph nodes Circulating blood → Spleen, thymus, and bone marrow Figure 5. T lymphocytes (orange), a type of white blood cell, attack a cancer cell (blue). LIVER AND BONE MARROW Preprocess B Lymphocytes LIVER - during midfetal life BONE MARROW - during late fetal life and after birth Figure 2. Formation of antibodies and sensitized lymphocytes by a lymph node in response to antigens B lymphocytes are different from T lymphocytes in two ways: 1. Actively secrete antibodies that are the reactive agents (large THYMUS GLAND proteins) that are capable of combining with and destroying the Preprocesses T Lymphocytes antigenic substance One thymic lymphocyte develops specific reactivity against one 2. Forms millions of types of B-lymphocyte antibodies with different antigen specific reactivities The only cells that are finally released are those that are non reactive against the body’s own antigens B LYMPHOCYTE These different types of preprocessed T lymphocytes leave the An antigen activates only the lymphocytes that have cell surface thymus and spread via the blood throughout the body to lodge in receptors that are complementary and recognize a specific antigen. lymphoid tissue everywhere Most of the preprocessing of T lymphocytes in the thymus occurs shortly before the birth of a baby and for a few months after birth. Beyond this period, removal of the thymus gland diminishes (but does not eliminate) the T-lymphocytic immune system. Removal of the thymus several months before birth can prevent development of all cell-mediated immunity, including rejection of transplanted organs. Figure 6. An antigen activates only the lymphocytes that have cell surface receptors that are complementary and recognize a specific antigen. Millions of Figure 3. Left: Location of thymus in the body. Right: Path of B cells different clones of lymphocytes exist (shown as B1, B2, and B3). When the and T cells for maturation lymphocyte clone (B2 in this example) is activated by its antigen, it reproduces to form large numbers of duplicate lymphocytes, which then secrete antibodies. Page 2 of 9 [PHYSIO] 1.06 RESISTANCE OF THE BODY TO INFECTION: Immunity and Allergy – Dr. Kristen Benedict B. Figuerres E. MECHANISM FOR ACTIVATING LYMPHOCYTE CLONES Each clone of lymphocytes is responsive to only a single type of antigen (or to several similar antigens that have almost exactly the same stereochemical characteristics). The reason for this is the following. In the case of the B lymphocytes, each of these has on its cell surface membrane about 100,000 antibody molecules that will react highly specifically with only one type of antigen. Therefore, when the appropriate antigen comes along, it immediately attaches to the antibody in the cell membrane; this leads to the activation process, described in more detail subsequently. In the case of the T lymphocytes, molecules similar to antibodies, called surface receptor proteins (or T-cell receptors), are on the surface of the T-cell Figure 9. Process of Cell-Mediated Immunity. membrane, and these are also highly specific for one specified activating antigen. An antigen therefore stimulates only those cells Role of T Cells in Activation of B Lymphocytes that have complementary receptors for the antigen and are already T-helper cells secrete lymphokines that activate the specific B committed to respond to it. lymphocytes. without the aid of these T-helper cells, the quantity of antibodies formed by the B lymphocytes is usually small Figure 7. Structure of B cell and T cell receptor. Role of Macrophages in the Activation Process macrophages line the sinusoids of the lymph nodes, spleen, and other lymphoid tissue Most invading organisms are first phagocytized and partially digested by the macrophages, and the antigenic products are liberated into the macrophage cytosol. Figure 10. Mechanism of B cell activation by T-helper cells. G. HUMORAL IMMUNITY AND ANTIBODIES Antibody Formation by Plasma Cells. ○ Before exposure to a specific antigen, the clones of B lymphocytes remain dormant in the lymphoid tissue. On entry of a foreign antigen, macrophages in lymphoid tissue phagocytize the antigen and then present it to adjacent B lymphocytes. In addition, the antigen is presented to T cells at the same time, and activated T-helper cells are formed. These helper cells also contribute to extreme activation of the B lymphocytes, as discussed later. Figure 8. Process in the engulfment of bacteria by macrophages F. CELL-MEDIATED IMMUNITY Most invading organisms are first phagocytized and partially digested by the macrophages, and the antigenic products are liberated into the macrophage cytosol. The macrophages then pass these antigens by cell to cell contact directly to the lymphocytes, thus leading to activation of the specified lymphocytic clones. The macrophages, in addition, secrete a special activating substance, interleukin-1, that promotes still further growth and reproduction of the specific lymphocytes. Figure 11. Processes in the primary immune response. Page 3 of 9 [PHYSIO] 1.06 RESISTANCE OF THE BODY TO INFECTION: Immunity and Allergy – Dr. Kristen Benedict B. Figuerres ANTIBODY FORMATION BY PLASMA CELLS VARIABLE PORTION - different for each specific antibody, and it is B lymphocytes → lymphoblasts → plasmablasts this portion that attaches specifically to a particular type of antigen ↓ CONSTANT PORTION - determines other properties of the antibody, Plasmablasts divide at a rate of about once every 10 hours for about nine establishing such factors as antibody diffusivity in the tissues, divisions, giving a total population of about 500 cells for each original adherence to specific structures in the tissues, attachment to the plasmablast in 4 days. complement complex, ease with which the antibodies pass through ↓ membranes, and other biological properties of the antibody Mature plasma cell then produces gamma globulin antibodies at an extremely A combination of noncovalent and covalent bonds (disulfide) holds rapid rate—about 2000 molecules per second for each plasma cell the light and heavy chains together. ↓ Antibodies are secreted into the lymph and carried to the circulating blood ↓ Continues for several days or weeks ↓ Exhaustion and death of the plasma cells FORMATION OF MEMORY CELLS Few of the lymphoblasts ↓ Form moderate numbers of Memory Cells ↓ Subsequent exposure to the same antigen will cause a much more rapid and potent antibody response because there are many more memory cells than there were original B lymphocytes of the specific clone. Figure 13. Structure of the typical IgG antibody. It is composed of two heavy FORMATION OF MEMORY CELLS polypeptide chains and two light polypeptide chains. The antigen attaches at The increased potency and duration of the secondary response two differents on the variable portions of the chains. explain why immunization is usually accomplished by injecting antigen in multiple doses, with periods of several weeks or several SPECIFICITY OF ANTIBODIES months between injections. Each antibody is specific for a particular antigen When the antibody is highly specific, there are so many bonding sites that the antibody-antigen coupling is exceedingly strong, held together by: 1. Hydrophobic bonding 2. Hydrogen bonding 3. Ionic attractions 4. Van der waals forces Obeys the thermodynamic mass action law: Figure 12. Time course of the antibody response in the circulating blood to a primary injection of antigen and to a secondary injection after several weeks. ○ Ka is called the affinity constant and is a measure of how tightly the antibody binds with the antigen. Generation of Lifelong Immunity by Plasma Cells ○ Law states that the rate of any chemical reaction is They differentiate into short-lived or long-lived plasma cells that proportional to the product of the masses of the reacting produce large amounts of antibodies. The short-lived plasma cells substances, with each mass raised to a power equal to the provide rapid protection but undergo apoptosis after a few days of coefficient that occurs in the chemical equation. intense antibody secretion. The long-lived plasma cells reside in tissues such as the bone marrow FIVE GENERAL CLASSES OF ANTIBODIES and gut-associated lymphoid tissue (GALT) and can continue IgM, IgG, IgA, IgD, and IgE producing antibodies for many years, providing lifelong immunity IgG - a bivalent antibody and constitutes about 75% of the antibodies against infectious diseases such as measles and smallpox. of the normal person, main antibody of the secondary response Thus, plasma cells that produce virus-neutralizing antibodies can be IgE - constitutes only a small percentage of the antibodies but is sustained for many decades after exposure, even into the tenth especially involved in allergies decade of life in humans. IgM - large share of the antibodies formed during the primary High titers of smallpox-specific antibodies, for example, have been response detected in the blood of subjects vaccinated in childhood, 70 years IgA - antibody in secretions (mucus, tears, saliva, colostrum) previously. Also, older survivors of the 1918 H1N1 influenza virus IgD - antibody of allergic and antiparasitic activity pandemic were shown to possess highly functional, virus-neutralizing antibodies to this virulent virus 90 years after they were infected. MECHANISMS OF ACTION OF ANTIBODIES Two ways to protect the body against invading agents: IMMUNOGLOBULINS (Igs) 1. By direct attack on the invader have molecular weights between 160,000 and 970,000 and 2. By activation of the Complement System constitute about 20% of all the plasma proteins composed of combinations of light and heavy polypeptide chains 1. DIRECT ACTION OF ANTIBODIES ON INVADING AGENTS Inactivation of the invading agent in one of several ways: Page 4 of 9 [PHYSIO] 1.06 RESISTANCE OF THE BODY TO INFECTION: Immunity and Allergy – Dr. Kristen Benedict B. Figuerres 1. AGGLUTINATION - in which multiple large particles with 4. Neutralization of Viruses antigens on their surfaces (e.g., bacteria or red cells) are bound 5. Chemotaxis together into a clump 6. Activation of Mast Cells and Basophils 2. PRECIPITATION - in which the molecular complex of soluble 7. Inflammatory Effects antigen (e.g., tetanus toxin) and antibody becomes so large that it is rendered insoluble and precipitates Release of Activated T Cells From Lymphoid Tissue and Formation of Memory 3. NEUTRALIZATION - in which the antibodies cover the toxic sites Cells of the antigenic agent On exposure to the proper antigen, as presented by adjacent 4. LYSIS - in which some potent antibodies are occasionally macrophages, the T lymphocytes of a specific lymphocyte clone capable of directly attacking membranes of cellular agents and proliferate and release large numbers of activated, specifically thereby cause rupture of the agent reacting T cells in ways that parallel antibody release by activated B These direct actions of antibodies often are not strong enough to cells. play a major role in protecting the body against the invader. Most of T-lymphocyte Memory Cells are formed in the same way that B the protection occurs through the amplifying effects of the Memory Cells are formed in the antibody system. complement system T CELLS - Play a major role in helping eliminate invading pathogens - Usually begin the process and assist in the acquired immune responses - There are as many as 100,000 receptor sites on a single T cell H. MAJOR HISTOCOMPATIBILITY COMPLEX PROTEINS T lymphocytes respond to antigens only when they are bound to specific molecules called MHC proteins on the surface of antigen-presenting cells in the lymphoid tissues Figure 14. Binding of the molecules of antigen to one another by bivalent antibodies 2. COMPLEMENT SYSTEM FOR ANTIBODY ACTION The main function of the complement system is to enhance (complement) the actions of antibodies and phagocytic cells in neutralizing and destroying pathogens, removing damaged cells from the body, and promoting inflammation. Complement is a collective term that describes a system of about 20 proteins, many of which are enzyme precursors. The principal actors in this system are 11 proteins designated C1 through C9, B, and D Figure 16. T cell activation needs the interaction of T-cell receptors with antigen All these are present normally among the plasma proteins in the (foreign protein) that is transported to the surface of the antigen-presenting cell blood, as well as among the proteins that leak out of the capillaries by a major histocompatibility complex (MHC) protein. These cell-to-cell adhesion into the tissue spaces. proteins allow the T cell to bind to the antigen-presenting cell long enough to be The enzyme precursors are normally inactive but can be activated by activated. the so-called Classical Pathway. THREE MAJOR TYPES OF ANTIGEN-PRESENTING CELLS (APCs) 1. MACROPHAGES CLASSICAL PATHWAY 2. B LYMPHOCYTES 3. DENDRITIC CELLS DENDRITIC CELLS Also known as “accessory cells” The most potent of the antigen-presenting cells Located throughout the body Main function is to present antigens to T cells The interaction of cell adhesion proteins is critical in permitting the T cells to bind to antigen-presenting cells long enough to become activated MAJOR HISTOCOMPATIBILITY COMPLEX (MHC) MHC proteins bind peptide fragments of antigen proteins that are degraded inside antigen-presenting cells and then transport them to the cell surface. TWO TYPES OF MHC PROTEINS Figure 15. Cascade of reactions during activation of the classical pathway of MHC I Proteins - present antigens to cytotoxic T cells (CD8) complement. MHC II Proteins - present antigens to T-helper cells (CD4) IMPORTANT EFFECTS OF THE CLASSICAL PATHWAY Remember: 1. Opsonization and Phagocytosis 2 to help, 1 to kill 2. Lysis MHC II - CD4 T Helper Cells; MHC I - CD8 Cytotoxic T Cells 3. Agglutination Page 5 of 9 [PHYSIO] 1.06 RESISTANCE OF THE BODY TO INFECTION: Immunity and Allergy – Dr. Kristen Benedict B. Figuerres infectious disease, therefore leading to the now well-known debilitating and lethal effects of acquired immunodeficiency syndrome (AIDS). CYTOTOXIC T CELLS direct attack cell that is capable of killing microorganisms and, at times, even some of the body’s own cells (killer cells). Figure 17. Mechanisms of T cell activation by the MHC proteins. DIFFERENT TYPES OF T CELLS AND THEIR FUNCTIONS 1. T-HELPER CELLS 2. CYTOTOXIC T CELLS 3. REGULATORY T CELLS (also called SUPPRESSOR T CELLS). FIgure 18. Sensitized lymphocytes (cytotoxic T cells) directly destructing an T-HELPER CELLS invading cell. the most numerous of the T cells (>75%) they help in the functions of the immune system in many ways The cytotoxic T cell secretes hole-forming proteins, called perforins, the major regulator of virtually all immune functions that literally punch round holes in the membrane of the attacked cell. forms a series of protein mediators, called lymphokines, that act on Fluid then flows rapidly into the cell from the interstitial space. In other cells of the immune system, as well as on bone marrow cells addition, the cytotoxic T cell releases cytotoxic substances directly into the attacked cell. Almost immediately, the attacked cell becomes greatly swollen, and it usually dissolves shortly thereafter. Figure 18. Mechanism of T-helper cells in activating cytotoxic T cells. Naïve CD4+ T-helper cells can differentiate into subset When stimulated, naïve CD4+ T-helper cells can differentiate into Figure 19. Mechanism of the destruction of the infected cell by cytotoxic T cells. subsets that produce different lymphokines and perform different functions. The cytotoxic cells also play an important role in destroying cancer cells, heart transplant cells, or other types of cells that are foreign to Table 2. Subsets of T-helper cells the person’s own body. Specific Regulatory Functions of Lymphokines 1. Stimulation of Growth and Proliferation of Cytotoxic T Cells and Regulatory T Cells 2. Stimulation of B-Cell Growth and Differentiation to Form Plasma Cells and Antibodies 3. Activation of the Macrophage System 4. Feedback Stimulatory Effect on T-Helper Cells In the absence of the lymphokines from the T-helper cells, the remainder of the immune system is almost paralyzed. It is the T-helper cells that are inactivated or destroyed by the Figure 20. Mechanism of the destruction of tumor cells by cytotoxic T cells. human immunodeficiency virus (HIV), specifically the CD4 T helper cells, which leaves the body almost totally unprotected against Page 6 of 9 [PHYSIO] 1.06 RESISTANCE OF THE BODY TO INFECTION: Immunity and Allergy – Dr. Kristen Benedict B. Figuerres REGULATORY T CELLS suppress the functions of both cytotoxic and T-helper cells Figure 21. Simplified illustration of the function of Regulatory T cells. TOLERANCE OF ACQUIRED IMMUNITY SYSTEM TO THE BODY’S OWN TISSUES develop during the preprocessing of T lymphocytes in the thymus Figure 23. Signs and symptoms of rheumatic fever. and of B lymphocytes in the bone marrow injecting a strong antigen into a fetus while the lymphocytes are 2. One type of Glomerulonephritis being preprocessed in these two areas prevents development of the person becomes immunized against the basement membranes of clones of lymphocytes in the lymphoid tissue that are specific for the glomeruli injected antigen 3. Myasthenia Gravis FAILURE OF THE TOLERANCE MECHANISM CAUSES AUTOIMMUNE DISEASES a neuromuscular disorder characterized by weakness and fatigability This phenomenon occurs to a greater extent the older a person of skeletal muscles becomes immunity develops against the acetylcholine receptor proteins of the usually occurs after destruction of some of the body’s own tissues, neuromuscular junction, causing paralysis which releases considerable quantities of self-antigens that circulate in the body and presumably cause acquired immunity in the form of activated T cells or antibodies Figure 24. Neuromuscular junction in Myasthenia Gravis. 4. Multiple Sclerosis (MS) lesions (plaque) in white matter of the brain and spinal cord resulting in the progressive destruction of myelin sheath axons the immune system attacks the myelin that covers nerve fibers, disrupting nervous system communication Figure 22. Different autoimmune diseases. EXAMPLES OF AUTOIMMUNE DISEASES 1. Rheumatic fever the body becomes immunized against tissues in the joints and heart, especially the heart valves, after exposure to a specific type of streptococcal toxin that has an epitope in its molecular structure similar to the structure of some of the body’s own self-antigens Figure 25. Demyelination of nerve fibers caused by the body’s immune system. 5. Systemic Lupus Erythematosus (SLE) a chronic, systemic inflammatory disease marked by alternating exacerbations and remissions Page 7 of 9 [PHYSIO] 1.06 RESISTANCE OF THE BODY TO INFECTION: Immunity and Allergy – Dr. Kristen Benedict B. Figuerres the person becomes immunized against many different body tissues the lungs to cause lung edema or asthmatic attacks in the case of at the same time some airborne antigens A disease that causes extensive damage and even death when SLE is POISON IVY severe. ○ The toxin of poison ivy in itself does not cause much harm to the peak age of onset: 20-40 years old tissues. more prevalent in women than men (10:1) ; worse during pregnancy ○ Upon repeated exposure, it does cause the formation of activated helper and cytotoxic T cells. ○ After subsequent exposure to the poison ivy toxin, within a day or so, the activated T cells diffuse from the circulating blood in large numbers into the skin to respond to the poison ivy toxin. ○ These T cells elicit a cell-mediated type of immune reaction. ○ Release of many toxic substances from the activated T cells, as well as extensive invasion of the tissues by macrophages along with their subsequent effects, one can well understand that the eventual result of some delayed reaction allergies can be serious tissue damage. ATOPIC ALLERGIES ASSOCIATED WITH EXCESS IgE ANTIBODIES The allergic tendency is genetically passed from parent to child and is characterized by the presence of large quantities of IgE antibodies in Figure 26. Symptoms of SLE. the blood IgE antibodies (the reagins) is a strong propensity to attach to mast cells and basophils I. IMMUNIZATION BY INJECTION OF ANTIGENS A person can be immunized by injecting dead organisms that are no longer capable of causing disease but that still have some of their chemical antigens. ○ Examples: typhoid fever, whooping cough, diphtheria, and many other types of bacterial diseases Immunity can be achieved against toxins that have been treated with chemicals so that their toxic nature has been destroyed, even though their antigens for causing immunity are still intact ○ Examples: tetanus, botulism, and other similar toxic diseases being infected with live organisms that have been attenuated these organisms have been grown in special culture media or have been passed through a series of animals until they have mutated enough that they will not cause disease but do still carry specific Figure 27. Structure of a Mast cell. antigens required for immunization ○ Examples: smallpox, yellow fever, poliomyelitis, measles, mast cells and basophils rupture → histamine, protease, and many other viral diseases slow-reacting substance of anaphylaxis (a mixture of toxic Attenuated- having been reduced in force, effect, or value. leukotrienes), eosinophil chemotactic substance, neutrophil chemotactic substance, heparin, and platelet-activating factors → J. PASSIVE IMMUNITY dilation of the local blood vessels, attraction of eosinophils and This temporary immunity is achieved by infusing antibodies, neutrophils to the reactive site, increased permeability of the activated T cells, or both obtained from the blood of someone else or capillaries with loss of fluid into the tissues, and contraction of local from some other animal that has been actively immunized against smooth muscle cells the antigen Antibodies last in the body of the recipient for 2 to 3 weeks ANAPHYLAXIS if the basophils and mast cells have been sensitized by the III. ALLERGY attachment of IgE reagins Histamine is released into the circulation and causes body-wide vasodilation, as well as increased permeability of the capillaries, with ALLERGY AND HYPERSENSITIVITY a resultant marked loss of plasma from the circulation 1. Allergy cause by activated T Cells: delayed-reaction allergy Occasionally a person who experiences this reaction dies of 2. Atopic allergies associated with excess IgE antibodies - caused by a circulatory shock within a few minutes unless treated with non ordinary response of the immune system. epinephrine to counteract the effects of the histamin 3. Anaphylaxis - widespread allergic reaction Also released from the activated basophils and mast cells is a mixture 4. Urticaria — localized anaphylactoid reactions of leukotrienes called slow-reacting substance of anaphylaxis. These 5. Hay Fever leukotrienes can cause spasm of the smooth muscle of the 6. Asthma bronchioles, eliciting an asthma-like attack and sometimes causing death by suffocation ALLERGY CAUSED BY ACTIVATED T CELLS: DELAYED-REACTION ALLERGY ○ caused by activated T cells ○ on repeated exposure, it does cause the formation of activated helper and cytotoxic T cells ○ The damage normally occurs in the tissue area where the instigating antigen is present, such as in the skin in the case of poison ivy or in Page 8 of 9 [PHYSIO] 1.06 RESISTANCE OF THE BODY TO INFECTION: Immunity and Allergy – Dr. Kristen Benedict B. Figuerres FIgure 30. The smooth muscles of a normal airway, an asthmatic airway, and an asthmatic airway during an attack. References: Figure 28. Symptoms of an allergic reaction. Hall, J. E., & Guyton, A. C. (2016). Guyton and Hall Textbook of Medical Physiology. Elsevier. URTICARIA Turgeon, M.L (2014) Immunology & Serology in Laboratory Medicine. 5th Ed. results from antigen entering specific skin areas and causing localized anaphylactoid reactions Histamine released locally causes: ○ vasodilation that induces an immediate red flare; and ○ increased local permeability of the capillaries that leads to local circumscribed areas of swelling of the skin within another few minutes The swellings are commonly called hives. Administration of antihistamine drugs to a person before exposure will prevent the hives. Figure 29. Hives on the body. HAY FEVER the allergen-reagin reaction occurs in the nose Histamine released local intranasal vascular dilation increased capillary pressure and increased capillary permeability rapid fluid leakage nasal linings become swollen and secretory Here again, the use of antihistamine drugs can prevent this swelling reaction. However, other products of the allergen-reagin reaction can still cause irritation of the nose, eliciting the typical sneezing syndrome Hay fever or allergic rhinitis ASTHMA Here again, the use of antihistamine drugs can prevent this swelling reaction. However, other products of the allergen-reagin reaction can still cause irritation of the nose, eliciting the typical sneezing syndrome. Page 9 of 9