Allergic Contact Dermatitis

Chapter 8 This chapter outlines the different types of immune system alterations, specifically hypersensitivity reactions and deficiencies in immunity. Hypersensitivity reactions can be categorized by the immunologic mechanism causing the disease and the source of the antigen being attacked by the immune system. There are four main types of hypersensitivity reactions: type I (IgE-mediated reactions), type II (tissue-specific reactions), type III (immune complex-mediated reactions), and type IV (cell-mediated reactions). Allergic Contact Dermatitis Environmental antigens, called haptens, become immunogenic by binding to larger proteins (carriers) The antigen urushiol from poison ivy reacts with normal skin proteins and triggers a cellmediated immune response Allergic contact dermatitis can be caused by exposure to industrial chemicals, cosmetics, detergents, clothing, food, metals, and topical medicines Quick Check 8.1 Distinguishing the four types of hypersensitivity mechanisms Mechanism of anaphylaxis Clinical examples of type IV hypersensitivity Allergy Hypersensitivity to environmental antigens (atopy) Allergies Allergies are hypersensitivity reactions to antigens that are not naturally found in the individual Most common allergies are type I reactions with mild symptoms like rhinitis and sneezing, but can be life-threatening in some cases (anaphylaxis) Allergens that cause allergic responses include pollens, molds, foods, animals, cigarette smoke, and components of house dust Bee Sting Allergy Bee venoms contain allergens that can cause a type I hypersensitivity reaction Symptoms of bee sting allergy can include swelling at the sting site, hives, itching, swelling in other areas of the body, and systemic symptoms like flushing, sweating, dizziness, and headache Severe reactions can result in gastrointestinal, respiratory, and vascular symptoms, which can be life-threatening Lifestyle changes for individuals with bee sting allergies include avoiding stinging or biting insects Carrying self-injectable epinephrine (EpiPen) is important to reverse severe symptoms Clinical desensitization to allergens can be achieved in some individuals, but it can also trigger severe and life-threatening systemic anaphylaxis Promising trials are underway for desensitization by oral or sublingual administration of increasing amounts of allergen for food allergies Autoimmunity Autoimmunity is a disturbance in the immune system's tolerance of self-antigens Autoimmune diseases occur when the immune system reacts against self-antigens, causing damage to the individual's tissues Many clinical disorders, collectively known as autoimmune diseases, are associated with autoimmunity Examples of Autoimmune Diseases Hyperthyroidism (Graves disease) Probable self-antigen: Receptors for thyroid-stimulating hormone Autoimmune Diseases Himoto hypothyroidism: Thyroid gland, Thyroid cell surface antigens, thyroglobulin Insulin-dependent diabetes: Pancreas, Islet cells, insulin, insulin receptors on pancreatic cells Addison disease: Adrenal gland, Surface antigens on steroid-producing cells, microsomal antigens Male infertility: Testis, Surface antigens on spermatozoa Pemphigus vulgaris: Skin, Intercellular substances in stratified squamous epithelium Bullous pemphigoid: Skin, Basement membrane Vitiligo: Skin, Surface antigens on melanocytes (melanin-producing cells) Multiple sclerosis: Neural tissue, Surface antigens of nerve cells Myasthenia gravis: Neuromuscular, Acetylcholine receptors, striations of skeletal and cardiac muscle Rheumatic heart disease: Heart, Cardiac tissue antigens that cross-react with group A streptococcal antigen Cardiomyopathy: Heart, Cardiac muscle Ulcerative colitis: Colon, Mucosal cells Pernicious anemia: Stomach, Surface antigens of parietal cells, intrinsic factor Primary biliary cirrhosis: Liver, Cells of bile duct Chronic active hepatitis: Liver, Surface antigens of hepatocytes, nuclei, microsomes, smooth muscle Sjögren syndrome: Eye, Antigens of lacrimal gland, salivary gland, thyroid, and nuclei of cells Ankylosing spondylitis: Connective tissue, Sacroiliac and spinal apophyseal joint Rheumatoid arthritis: Joints, Collagen, immunoglobulin G (IgG) Systemic lupus erythematosus: Multiple sites, Numerous antigens in nuclei, organelles, and extracellular matrix Immune complex glomerulonephritis: Kidney, Numerous immune complexes deposited in glomerular vessels Goodpasture syndrome: Kidney, Glomerular basement membrane Idiopathic neutropenia: Hematologic system, Surface antigens on polymorphonuclear neutrophils Idiopathic lymphopenia: Hematologic system, Surface antigens on lymphocytes Autoimmune hemolytic anemia: Hematologic system, Surface antigens on erythrocytes Autoimmune thrombocytopenic purpura: Hematologic system, Surface antigens on platelets Goodpasture syndrome: Respiratory system, Septal membrane of alveolus Breakdown of Tolerance An individual is usually tolerant to his or her own antigens Tolerance is a state of immunologic control so that the individual does not make a detrimental immune response against his or her own cells and tissues Autoimmune disease results from a breakdown of this tolerance The initiating event that breaks tolerance is unclear for most autoimmune diseases Potential infectious initiators of autoimmune disease are implicated for many autoimmune disorders Example: Acute rheumatic fever M proteins in the bacterial capsule mimic normal heart antigens and induce antibodies that also react with proteins in the heart valve Causes inflammation and damage to the valve Streptococcal Infections and Glomerulonephritis Some streptococcal infections release bacterial antigens into the blood These antigens form circulating immune complexes The complexes may deposit in the kidneys and cause immune complex-mediated glomerulonephritis Systemic Lupus Erythematosus (SLE) SLE is the most common and serious autoimmune disorder characterized by production of autoantibodies against self-antigens The autoantibodies react with circulating antigens and form circulating immune complexes Deposition of immune complexes in the kidneys can cause severe kidney inflammation Symptoms of SLE result from type III hypersensitivity reactions SLE occurs more often in women, especially in the 20-40 year age group Blacks have a higher risk compared to whites Clinical manifestations of SLE may wax and wane Symptoms include joint inflammation, rash, renal disease, hematologic abnormalities, and cardiovascular diseases