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Anatomy and Physiology

21.6 Diseases Associated with Depressed or Overactive Immune Responses

Anatomy and Physiology21.6 Diseases Associated with Depressed or Overactive Immune Responses
  1. Preface
  2. Unit 1: Levels of Organization
    1. 1 An Introduction to the Human Body
      1. Introduction
      2. 1.1 Overview of Anatomy and Physiology
      3. 1.2 Structural Organization of the Human Body
      4. 1.3 Functions of Human Life
      5. 1.4 Requirements for Human Life
      6. 1.5 Homeostasis
      7. 1.6 Anatomical Terminology
      8. 1.7 Medical Imaging
      9. Key Terms
      10. Chapter Review
      11. Interactive Link Questions
      12. Review Questions
      13. Critical Thinking Questions
    2. 2 The Chemical Level of Organization
      1. Introduction
      2. 2.1 Elements and Atoms: The Building Blocks of Matter
      3. 2.2 Chemical Bonds
      4. 2.3 Chemical Reactions
      5. 2.4 Inorganic Compounds Essential to Human Functioning
      6. 2.5 Organic Compounds Essential to Human Functioning
      7. Key Terms
      8. Chapter Review
      9. Interactive Link Questions
      10. Review Questions
      11. Critical Thinking Questions
    3. 3 The Cellular Level of Organization
      1. Introduction
      2. 3.1 The Cell Membrane
      3. 3.2 The Cytoplasm and Cellular Organelles
      4. 3.3 The Nucleus and DNA Replication
      5. 3.4 Protein Synthesis
      6. 3.5 Cell Growth and Division
      7. 3.6 Cellular Differentiation
      8. Key Terms
      9. Chapter Review
      10. Interactive Link Questions
      11. Review Questions
      12. Critical Thinking Questions
    4. 4 The Tissue Level of Organization
      1. Introduction
      2. 4.1 Types of Tissues
      3. 4.2 Epithelial Tissue
      4. 4.3 Connective Tissue Supports and Protects
      5. 4.4 Muscle Tissue and Motion
      6. 4.5 Nervous Tissue Mediates Perception and Response
      7. 4.6 Tissue Injury and Aging
      8. Key Terms
      9. Chapter Review
      10. Interactive Link Questions
      11. Review Questions
      12. Critical Thinking Questions
  3. Unit 2: Support and Movement
    1. 5 The Integumentary System
      1. Introduction
      2. 5.1 Layers of the Skin
      3. 5.2 Accessory Structures of the Skin
      4. 5.3 Functions of the Integumentary System
      5. 5.4 Diseases, Disorders, and Injuries of the Integumentary System
      6. Key Terms
      7. Chapter Review
      8. Interactive Link Questions
      9. Review Questions
      10. Critical Thinking Questions
    2. 6 Bone Tissue and the Skeletal System
      1. Introduction
      2. 6.1 The Functions of the Skeletal System
      3. 6.2 Bone Classification
      4. 6.3 Bone Structure
      5. 6.4 Bone Formation and Development
      6. 6.5 Fractures: Bone Repair
      7. 6.6 Exercise, Nutrition, Hormones, and Bone Tissue
      8. 6.7 Calcium Homeostasis: Interactions of the Skeletal System and Other Organ Systems
      9. Key Terms
      10. Chapter Review
      11. Review Questions
      12. Critical Thinking Questions
    3. 7 Axial Skeleton
      1. Introduction
      2. 7.1 Divisions of the Skeletal System
      3. 7.2 The Skull
      4. 7.3 The Vertebral Column
      5. 7.4 The Thoracic Cage
      6. 7.5 Embryonic Development of the Axial Skeleton
      7. Key Terms
      8. Chapter Review
      9. Interactive Link Questions
      10. Review Questions
      11. Critical Thinking Questions
    4. 8 The Appendicular Skeleton
      1. Introduction
      2. 8.1 The Pectoral Girdle
      3. 8.2 Bones of the Upper Limb
      4. 8.3 The Pelvic Girdle and Pelvis
      5. 8.4 Bones of the Lower Limb
      6. 8.5 Development of the Appendicular Skeleton
      7. Key Terms
      8. Chapter Review
      9. Interactive Link Questions
      10. Review Questions
      11. Critical Thinking Questions
    5. 9 Joints
      1. Introduction
      2. 9.1 Classification of Joints
      3. 9.2 Fibrous Joints
      4. 9.3 Cartilaginous Joints
      5. 9.4 Synovial Joints
      6. 9.5 Types of Body Movements
      7. 9.6 Anatomy of Selected Synovial Joints
      8. 9.7 Development of Joints
      9. Key Terms
      10. Chapter Review
      11. Interactive Link Questions
      12. Review Questions
      13. Critical Thinking Questions
    6. 10 Muscle Tissue
      1. Introduction
      2. 10.1 Overview of Muscle Tissues
      3. 10.2 Skeletal Muscle
      4. 10.3 Muscle Fiber Contraction and Relaxation
      5. 10.4 Nervous System Control of Muscle Tension
      6. 10.5 Types of Muscle Fibers
      7. 10.6 Exercise and Muscle Performance
      8. 10.7 Cardiac Muscle Tissue
      9. 10.8 Smooth Muscle
      10. 10.9 Development and Regeneration of Muscle Tissue
      11. Key Terms
      12. Chapter Review
      13. Interactive Link Questions
      14. Review Questions
      15. Critical Thinking Questions
    7. 11 The Muscular System
      1. Introduction
      2. 11.1 Interactions of Skeletal Muscles, Their Fascicle Arrangement, and Their Lever Systems
      3. 11.2 Naming Skeletal Muscles
      4. 11.3 Axial Muscles of the Head, Neck, and Back
      5. 11.4 Axial Muscles of the Abdominal Wall, and Thorax
      6. 11.5 Muscles of the Pectoral Girdle and Upper Limbs
      7. 11.6 Appendicular Muscles of the Pelvic Girdle and Lower Limbs
      8. Key Terms
      9. Chapter Review
      10. Review Questions
      11. Critical Thinking Questions
  4. Unit 3: Regulation, Integration, and Control
    1. 12 The Nervous System and Nervous Tissue
      1. Introduction
      2. 12.1 Basic Structure and Function of the Nervous System
      3. 12.2 Nervous Tissue
      4. 12.3 The Function of Nervous Tissue
      5. 12.4 The Action Potential
      6. 12.5 Communication Between Neurons
      7. Key Terms
      8. Chapter Review
      9. Interactive Link Questions
      10. Review Questions
      11. Critical Thinking Questions
    2. 13 Anatomy of the Nervous System
      1. Introduction
      2. 13.1 The Embryologic Perspective
      3. 13.2 The Central Nervous System
      4. 13.3 Circulation and the Central Nervous System
      5. 13.4 The Peripheral Nervous System
      6. Key Terms
      7. Chapter Review
      8. Interactive Link Questions
      9. Review Questions
      10. Critical Thinking Questions
    3. 14 The Somatic Nervous System
      1. Introduction
      2. 14.1 Sensory Perception
      3. 14.2 Central Processing
      4. 14.3 Motor Responses
      5. Key Terms
      6. Chapter Review
      7. Interactive Link Questions
      8. Review Questions
      9. Critical Thinking Questions
    4. 15 The Autonomic Nervous System
      1. Introduction
      2. 15.1 Divisions of the Autonomic Nervous System
      3. 15.2 Autonomic Reflexes and Homeostasis
      4. 15.3 Central Control
      5. 15.4 Drugs that Affect the Autonomic System
      6. Key Terms
      7. Chapter Review
      8. Interactive Link Questions
      9. Review Questions
      10. Critical Thinking Questions
    5. 16 The Neurological Exam
      1. Introduction
      2. 16.1 Overview of the Neurological Exam
      3. 16.2 The Mental Status Exam
      4. 16.3 The Cranial Nerve Exam
      5. 16.4 The Sensory and Motor Exams
      6. 16.5 The Coordination and Gait Exams
      7. Key Terms
      8. Chapter Review
      9. Interactive Link Questions
      10. Review Questions
      11. Critical Thinking Questions
    6. 17 The Endocrine System
      1. Introduction
      2. 17.1 An Overview of the Endocrine System
      3. 17.2 Hormones
      4. 17.3 The Pituitary Gland and Hypothalamus
      5. 17.4 The Thyroid Gland
      6. 17.5 The Parathyroid Glands
      7. 17.6 The Adrenal Glands
      8. 17.7 The Pineal Gland
      9. 17.8 Gonadal and Placental Hormones
      10. 17.9 The Endocrine Pancreas
      11. 17.10 Organs with Secondary Endocrine Functions
      12. 17.11 Development and Aging of the Endocrine System
      13. Key Terms
      14. Chapter Review
      15. Interactive Link Questions
      16. Review Questions
      17. Critical Thinking Questions
  5. Unit 4: Fluids and Transport
    1. 18 The Cardiovascular System: Blood
      1. Introduction
      2. 18.1 An Overview of Blood
      3. 18.2 Production of the Formed Elements
      4. 18.3 Erythrocytes
      5. 18.4 Leukocytes and Platelets
      6. 18.5 Hemostasis
      7. 18.6 Blood Typing
      8. Key Terms
      9. Chapter Review
      10. Interactive Link Questions
      11. Review Questions
      12. Critical Thinking Questions
    2. 19 The Cardiovascular System: The Heart
      1. Introduction
      2. 19.1 Heart Anatomy
      3. 19.2 Cardiac Muscle and Electrical Activity
      4. 19.3 Cardiac Cycle
      5. 19.4 Cardiac Physiology
      6. 19.5 Development of the Heart
      7. Key Terms
      8. Chapter Review
      9. Interactive Link Questions
      10. Review Questions
      11. Critical Thinking Questions
    3. 20 The Cardiovascular System: Blood Vessels and Circulation
      1. Introduction
      2. 20.1 Structure and Function of Blood Vessels
      3. 20.2 Blood Flow, Blood Pressure, and Resistance
      4. 20.3 Capillary Exchange
      5. 20.4 Homeostatic Regulation of the Vascular System
      6. 20.5 Circulatory Pathways
      7. 20.6 Development of Blood Vessels and Fetal Circulation
      8. Key Terms
      9. Chapter Review
      10. Interactive Link Questions
      11. Review Questions
      12. Critical Thinking Questions
    4. 21 The Lymphatic and Immune System
      1. Introduction
      2. 21.1 Anatomy of the Lymphatic and Immune Systems
      3. 21.2 Barrier Defenses and the Innate Immune Response
      4. 21.3 The Adaptive Immune Response: T lymphocytes and Their Functional Types
      5. 21.4 The Adaptive Immune Response: B-lymphocytes and Antibodies
      6. 21.5 The Immune Response against Pathogens
      7. 21.6 Diseases Associated with Depressed or Overactive Immune Responses
      8. 21.7 Transplantation and Cancer Immunology
      9. Key Terms
      10. Chapter Review
      11. Interactive Link Questions
      12. Review Questions
      13. Critical Thinking Questions
  6. Unit 5: Energy, Maintenance, and Environmental Exchange
    1. 22 The Respiratory System
      1. Introduction
      2. 22.1 Organs and Structures of the Respiratory System
      3. 22.2 The Lungs
      4. 22.3 The Process of Breathing
      5. 22.4 Gas Exchange
      6. 22.5 Transport of Gases
      7. 22.6 Modifications in Respiratory Functions
      8. 22.7 Embryonic Development of the Respiratory System
      9. Key Terms
      10. Chapter Review
      11. Interactive Link Questions
      12. Review Questions
      13. Critical Thinking Questions
    2. 23 The Digestive System
      1. Introduction
      2. 23.1 Overview of the Digestive System
      3. 23.2 Digestive System Processes and Regulation
      4. 23.3 The Mouth, Pharynx, and Esophagus
      5. 23.4 The Stomach
      6. 23.5 The Small and Large Intestines
      7. 23.6 Accessory Organs in Digestion: The Liver, Pancreas, and Gallbladder
      8. 23.7 Chemical Digestion and Absorption: A Closer Look
      9. Key Terms
      10. Chapter Review
      11. Interactive Link Questions
      12. Review Questions
      13. Critical Thinking Questions
    3. 24 Metabolism and Nutrition
      1. Introduction
      2. 24.1 Overview of Metabolic Reactions
      3. 24.2 Carbohydrate Metabolism
      4. 24.3 Lipid Metabolism
      5. 24.4 Protein Metabolism
      6. 24.5 Metabolic States of the Body
      7. 24.6 Energy and Heat Balance
      8. 24.7 Nutrition and Diet
      9. Key Terms
      10. Chapter Review
      11. Review Questions
      12. Critical Thinking Questions
    4. 25 The Urinary System
      1. Introduction
      2. 25.1 Physical Characteristics of Urine
      3. 25.2 Gross Anatomy of Urine Transport
      4. 25.3 Gross Anatomy of the Kidney
      5. 25.4 Microscopic Anatomy of the Kidney
      6. 25.5 Physiology of Urine Formation
      7. 25.6 Tubular Reabsorption
      8. 25.7 Regulation of Renal Blood Flow
      9. 25.8 Endocrine Regulation of Kidney Function
      10. 25.9 Regulation of Fluid Volume and Composition
      11. 25.10 The Urinary System and Homeostasis
      12. Key Terms
      13. Chapter Review
      14. Review Questions
      15. Critical Thinking Questions
    5. 26 Fluid, Electrolyte, and Acid-Base Balance
      1. Introduction
      2. 26.1 Body Fluids and Fluid Compartments
      3. 26.2 Water Balance
      4. 26.3 Electrolyte Balance
      5. 26.4 Acid-Base Balance
      6. 26.5 Disorders of Acid-Base Balance
      7. Key Terms
      8. Chapter Review
      9. Interactive Link Questions
      10. Review Questions
      11. Critical Thinking Questions
  7. Unit 6: Human Development and the Continuity of Life
    1. 27 The Reproductive System
      1. Introduction
      2. 27.1 Anatomy and Physiology of the Male Reproductive System
      3. 27.2 Anatomy and Physiology of the Female Reproductive System
      4. 27.3 Development of the Male and Female Reproductive Systems
      5. Key Terms
      6. Chapter Review
      7. Interactive Link Questions
      8. Review Questions
      9. Critical Thinking Questions
    2. 28 Development and Inheritance
      1. Introduction
      2. 28.1 Fertilization
      3. 28.2 Embryonic Development
      4. 28.3 Fetal Development
      5. 28.4 Maternal Changes During Pregnancy, Labor, and Birth
      6. 28.5 Adjustments of the Infant at Birth and Postnatal Stages
      7. 28.6 Lactation
      8. 28.7 Patterns of Inheritance
      9. Key Terms
      10. Chapter Review
      11. Interactive Link Questions
      12. Review Questions
      13. Critical Thinking Questions
  8. References
  9. Index
By the end of this section, you will be able to:
  • Discuss inherited and acquired immunodeficiencies
  • Explain the four types of hypersensitivity and how they differ
  • Give an example of how autoimmune disease breaks tolerance

This section is about how the immune system goes wrong. When it goes haywire, and becomes too weak or too strong, it leads to a state of disease. The factors that maintain immunological homeostasis are complex and incompletely understood.

Immunodeficiencies

As you have seen, the immune system is quite complex. It has many pathways using many cell types and signals. Because it is so complex, there are many ways for it to go wrong. Inherited immunodeficiencies arise from gene mutations that affect specific components of the immune response. There are also acquired immunodeficiencies with potentially devastating effects on the immune system, such as HIV.

Inherited Immunodeficiencies

A list of all inherited immunodeficiencies is well beyond the scope of this book. The list is almost as long as the list of cells, proteins, and signaling molecules of the immune system itself. Some deficiencies, such as those for complement, cause only a higher susceptibility to some Gram-negative bacteria. Others are more severe in their consequences. Certainly, the most serious of the inherited immunodeficiencies is severe combined immunodeficiency disease (SCID). This disease is complex because it is caused by many different genetic defects. What groups them together is the fact that both the B cell and T cell arms of the adaptive immune response are affected.

Children with this disease usually die of opportunistic infections within their first year of life unless they receive a bone marrow transplant. Such a procedure had not yet been perfected for David Vetter, the “boy in the bubble,” who was treated for SCID by having to live almost his entire life in a sterile plastic cocoon for the 12 years before his death from infection in 1984. One of the features that make bone marrow transplants work as well as they do is the proliferative capability of hematopoietic stem cells of the bone marrow. Only a small amount of bone marrow from a healthy donor is given intravenously to the recipient. It finds its own way to the bone where it populates it, eventually reconstituting the patient’s immune system, which is usually destroyed beforehand by treatment with radiation or chemotherapeutic drugs.

New treatments for SCID using gene therapy, inserting nondefective genes into cells taken from the patient and giving them back, have the advantage of not needing the tissue match required for standard transplants. Although not a standard treatment, this approach holds promise, especially for those in whom standard bone marrow transplantation has failed.

Human Immunodeficiency Virus/AIDS

Although many viruses cause suppression of the immune system, only one wipes it out completely, and that is the previously mentioned HIV. It is worth discussing the biology of this virus, which can lead to the well-known AIDS, so that its full effects on the immune system can be understood. The virus is transmitted through semen, vaginal fluids, and blood, and can be caught by risky sexual behaviors and the sharing of needles by intravenous drug users. There are sometimes, but not always, flu-like symptoms in the first 1 to 2 weeks after infection. This is later followed by seroconversion. The anti-HIV antibodies formed during seroconversion are the basis for most initial HIV screening done in the United States. Because seroconversion takes different lengths of time in different individuals, multiple AIDS tests are given months apart to confirm or eliminate the possibility of infection.

After seroconversion, the amount of virus circulating in the blood drops and stays at a low level for several years. During this time, the levels of CD4+ cells, especially helper T cells, decline steadily, until at some point, the immune response is so weak that opportunistic disease and eventually death result. HIV uses CD4 as the receptor to get inside cells, but it also needs a co-receptor, such as CCR5 or CXCR4. These co-receptors, which usually bind to chemokines, present another target for anti-HIV drug development. Although other antigen-presenting cells are infected with HIV, given that CD4+ helper T cells play an important role in T cell immune responses and antibody responses, it should be no surprise that both types of immune responses are eventually seriously compromised.

Treatment for the disease consists of drugs that target virally encoded proteins that are necessary for viral replication but are absent from normal human cells. By targeting the virus itself and sparing the cells, this approach has been successful in significantly prolonging the lives of HIV-positive individuals. On the other hand, an HIV vaccine has been 30 years in development and is still years away. Because the virus mutates rapidly to evade the immune system, scientists have been looking for parts of the virus that do not change and thus would be good targets for a vaccine candidate.

Hypersensitivities

The word “hypersensitivity” simply means sensitive beyond normal levels of activation. Allergies and inflammatory responses to nonpathogenic environmental substances have been observed since the dawn of history. Hypersensitivity is a medical term describing symptoms that are now known to be caused by unrelated mechanisms of immunity. Still, it is useful for this discussion to use the four types of hypersensitivities as a guide to understand these mechanisms (Figure 21.28).

This table describes different types of hypersensitivity. In Type I (IgE-Mediated Hypersensitivity), IgE is bound to mast cells via its Fc portion. When an allergen binds to these antibodies, crosslinking of IgE induces degranulation. Type I causes localized and systemic anaphylaxis, seasonal allergies including hay fever, food allergies such as those to shellfish and peanuts, hives, and eczema. In Type II (IgG-Mediated Hypersensitivity), cells are destroyed by bound antibody, either by activation of complement or by a cytotoxic T cell with an Fc receptor for the antibody (ADCC). Examples are when red blood cells are destroyed by complement and antibody during a transfusion of mismatched blood types or during erythroblastosis fetalis. In Type III (Immune Complex-Mediated Hypersensitivity), antigen-antibody complexes are deposited in tissues, causing activation of complement, which attracts neutrophils to the site. Most common forms of immune complex disease are seen in glomerulonephritis, rheumatoid arthritis, and systemic lupus erythematosus. In Type IV (Cell-Mediated Hypersensitivity), Th1 cells secrete cytokines, which activate macrophages and cytotoxic T cells and can cause macrophage accumulation at the site. Most common forms are contact dermatitis, tuberculin reaction, and autoimmune diseases such as diabetes mellitus type I, multiple sclerosis, and rheumatoid arthritis.
Figure 21.28 Immune Hypersensitivity Components of the immune system cause four types of hypersensitivity. Notice that types I–III are B cell mediated, whereas type IV hypersensitivity is exclusively a T cell phenomenon.

Immediate (Type I) Hypersensitivity

Antigens that cause allergic responses are often referred to as allergens. The specificity of the immediate hypersensitivity response is predicated on the binding of allergen-specific IgE to the mast cell surface. The process of producing allergen-specific IgE is called sensitization, and is a necessary prerequisite for the symptoms of immediate hypersensitivity to occur. Allergies and allergic asthma are mediated by mast cell degranulation that is caused by the crosslinking of the antigen-specific IgE molecules on the mast cell surface. The mediators released have various vasoactive effects already discussed, but the major symptoms of inhaled allergens are the nasal edema and runny nose caused by the increased vascular permeability and increased blood flow of nasal blood vessels. As these mediators are released with mast cell degranulation, type I hypersensitivity reactions are usually rapid and occur within just a few minutes, hence the term immediate hypersensitivity.

Most allergens are in themselves nonpathogenic and therefore innocuous. Some individuals develop mild allergies, which are usually treated with antihistamines. Others develop severe allergies that may cause anaphylactic shock, which can potentially be fatal within 20 to 30 minutes if untreated. This drop in blood pressure (shock) with accompanying contractions of bronchial smooth muscle is caused by systemic mast cell degranulation when an allergen is eaten (for example, shellfish and peanuts), injected (by a bee sting or being administered penicillin), or inhaled (asthma). Because epinephrine raises blood pressure and relaxes bronchial smooth muscle, it is routinely used to counteract the effects of anaphylaxis and can be lifesaving. Patients with known severe allergies are encouraged to keep automatic epinephrine injectors with them at all times, especially when away from easy access to hospitals.

Allergists use skin testing to identify allergens in type I hypersensitivity. In skin testing, allergen extracts are injected into the epidermis, and a positive result of a soft, pale swelling at the site surrounded by a red zone (called the wheal and flare response), caused by the release of histamine and the granule mediators, usually occurs within 30 minutes. The soft center is due to fluid leaking from the blood vessels and the redness is caused by the increased blood flow to the area that results from the dilation of local blood vessels at the site.

Type II and Type III Hypersensitivities

Type II hypersensitivity, which involves IgG-mediated lysis of cells by complement proteins, occurs during mismatched blood transfusions and blood compatibility diseases such as erythroblastosis fetalis (see section on transplantation). Type III hypersensitivity occurs with diseases such as systemic lupus erythematosus, where soluble antigens, mostly DNA and other material from the nucleus, and antibodies accumulate in the blood to the point that the antigen and antibody precipitate along blood vessel linings. These immune complexes often lodge in the kidneys, joints, and other organs where they can activate complement proteins and cause inflammation.

Delayed (Type IV) Hypersensitivity

Delayed hypersensitivity, or type IV hypersensitivity, is basically a standard cellular immune response. In delayed hypersensitivity, the first exposure to an antigen is called sensitization, such that on re-exposure, a secondary cellular response results, secreting cytokines that recruit macrophages and other phagocytes to the site. These sensitized T cells, of the Th1 class, will also activate cytotoxic T cells. The time it takes for this reaction to occur accounts for the 24- to 72-hour delay in development.

The classical test for delayed hypersensitivity is the tuberculin test for tuberculosis, where bacterial proteins from M. tuberculosis are injected into the skin. A couple of days later, a positive test is indicated by a raised red area that is hard to the touch, called an induration, which is a consequence of the cellular infiltrate, an accumulation of activated macrophages. A positive tuberculin test means that the patient has been exposed to the bacteria and exhibits a cellular immune response to it.

Another type of delayed hypersensitivity is contact sensitivity, where substances such as the metal nickel cause a red and swollen area upon contact with the skin. The individual must have been previously sensitized to the metal. A much more severe case of contact sensitivity is poison ivy, but many of the harshest symptoms of the reaction are associated with the toxicity of its oils and are not T cell mediated.

Autoimmune Responses

The worst cases of the immune system over-reacting are autoimmune diseases. Somehow, tolerance breaks down and the immune systems in individuals with these diseases begin to attack their own bodies, causing significant damage. The trigger for these diseases is, more often than not, unknown, and the treatments are usually based on resolving the symptoms using immunosuppressive and anti-inflammatory drugs such as steroids. These diseases can be localized and crippling, as in rheumatoid arthritis, or diffuse in the body with multiple symptoms that differ in different individuals, as is the case with systemic lupus erythematosus (Figure 21.29).

The left panel of this figure shows an x-ray image of a person’s hand with rheumatoid arthritis, and the right panel of this figure shows a woman’s body with labels showing the different responses in the body when the patient suffers from lupus.
Figure 21.29 Autoimmune Disorders: Rheumatoid Arthritis and Lupus (a) Extensive damage to the right hand of a rheumatoid arthritis sufferer is shown in the x-ray. (b) The diagram shows a variety of possible symptoms of systemic lupus erythematosus.

Environmental triggers seem to play large roles in autoimmune responses. One explanation for the breakdown of tolerance is that, after certain bacterial infections, an immune response to a component of the bacterium cross-reacts with a self-antigen. This mechanism is seen in rheumatic fever, a result of infection with Streptococcus bacteria, which causes strep throat. The antibodies to this pathogen’s M protein cross-react with an antigenic component of heart myosin, a major contractile protein of the heart that is critical to its normal function. The antibody binds to these molecules and activates complement proteins, causing damage to the heart, especially to the heart valves. On the other hand, some theories propose that having multiple common infectious diseases actually prevents autoimmune responses. The fact that autoimmune diseases are rare in countries that have a high incidence of infectious diseases supports this idea, another example of the hygiene hypothesis discussed earlier in this chapter.

There are genetic factors in autoimmune diseases as well. Some diseases are associated with the MHC genes that an individual expresses. The reason for this association is likely because if one’s MHC molecules are not able to present a certain self-antigen, then that particular autoimmune disease cannot occur. Overall, there are more than 80 different autoimmune diseases, which are a significant health problem in the elderly. Table 21.7 lists several of the most common autoimmune diseases, the antigens that are targeted, and the segment of the adaptive immune response that causes the damage.

Autoimmune Diseases
Disease Autoantigen Symptoms
Celiac disease Tissue transglutaminase Damage to small intestine
Diabetes mellitus type I Beta cells of pancreas Low insulin production; inability to regulate serum glucose
Graves’ disease Thyroid-stimulating hormone receptor (antibody blocks receptor) Hyperthyroidism
Hashimoto’s thyroiditis Thyroid-stimulating hormone receptor (antibody mimics hormone and stimulates receptor) Hypothyroidism
Lupus erythematosus Nuclear DNA and proteins Damage of many body systems
Myasthenia gravis Acetylcholine receptor in neuromuscular junctions Debilitating muscle weakness
Rheumatoid arthritis Joint capsule antigens Chronic inflammation of joints
Table 21.7
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