Autoimmune Diseases: Videos & Practice Problems

Autoimmune diseases arise when the immune system mistakenly attacks self tissues via autoantibodies or autoreactive T cells, affecting humoral and cell-mediated immunity. These disorders can be organ-specific or systemic, including Graves' disease, multiple sclerosis, and systemic lupus erythematosus. Contributing factors include genetics, environmental triggers like infections mimicking host antigens, and immune regulation defects. Despite extensive research, no cures exist, highlighting the complexity of immune tolerance and self-recognition. Understanding these mechanisms is crucial for advancing immunotherapy and managing autoimmune pathogenesis within adaptive immunity frameworks.

Autoimmune Diseases

The immune system is designed to respond rapidly and recognize a vast array of potential threats, prioritizing speed and flexibility over perfect precision. This balance, while essential for defending against pathogens, sometimes leads to errors where the immune system mistakenly attacks the body's own tissues, resulting in autoimmune diseases. The term "autoimmune" derives from "auto," meaning self, highlighting that these conditions involve the immune system targeting self-antigens instead of foreign invaders.

Autoimmune diseases encompass over 100 distinct disorders, each relatively rare on its own, but collectively affecting an estimated 5 to 10 percent of the global population. This prevalence underscores the importance of understanding their underlying mechanisms. These diseases can arise from defects in humoral immunity, where plasma cells produce autoantibodies—antibodies directed against the body's own antigens (autoantigens). Alternatively, they may result from errors in cell-mediated immunity, involving autoreactive cytotoxic T cells that recognize self-antigens presented by MHC class I molecules on normal cells and subsequently destroy them. In some cases, both humoral and cell-mediated immune responses contribute to the pathology.

Autoantibodies bind to autoantigens on self tissues, leading to tissue damage, while autoreactive cytotoxic T cells release cytotoxic molecules that induce apoptosis in self cells. These mechanisms can cause autoimmune diseases that are either organ-specific, affecting a single tissue or organ, or systemic, impacting multiple systems throughout the body.

Understanding the balance between immune system responsiveness and self-tolerance is crucial for grasping how autoimmune diseases develop. The immune system’s need for rapid action against diverse threats sometimes compromises its ability to perfectly distinguish self from non-self, leading to these disorders. This knowledge forms the foundation for exploring specific autoimmune diseases and their treatments.

Which of the following statements is true about autoantigens?

• A. Autoantigens are molecules on the surfaces of self-cells which trigger apoptosis.
• B. Autoantigens are molecules on the surfaces of self-cells which are attacked by the immune system.
• C. Autoantigens are molecules on the surfaces of foreign cells which are attacked by the immune system.
• D. When injected into a new host, autoantigens are integrated into the host’s immune system.

Answer: (B)

Which of the following statements about autoimmune diseases is false?

• A. Some autoimmune diseases are organ- or tissue-specific, and some are systemic (affect the entire body).
• B. Autoimmune diseases occur when the immune system attacks the body’s own cells.
• C. Autoimmune diseases are triggered by plasma cells creating autoantibodies which bind to autoantigens.
• D. Autoimmune diseases occur when T cells recognize self-damaging immune cells & tag them for destruction.

Answer: (D)

Examples of Autoimmune Diseases

Autoimmune diseases occur when the immune system mistakenly attacks the body's own tissues, leading to various health complications. These diseases can be categorized into organ-specific autoimmune diseases, which affect localized areas, and systemic autoimmune diseases, which impact multiple organs throughout the body.

Graves' disease and myasthenia gravis are examples of organ-specific autoimmune disorders linked to type II hypersensitivity reactions. In Graves' disease, autoantibodies target hormone receptors on thyroid cells, causing overstimulation and excessive thyroid hormone production. Conversely, myasthenia gravis involves autoantibodies that block receptors at neuromuscular junctions, inhibiting muscle contractions and resulting in muscle weakness.

Multiple sclerosis (MS) and type 1 diabetes mellitus are autoimmune diseases associated with type IV hypersensitivity, characterized by delayed T cell-mediated immune responses. MS involves the immune system attacking the myelin sheath, the protective insulating layer around nerve axons in the brain and spinal cord, which disrupts nerve impulse conduction and impairs nervous system communication. Type 1 diabetes mellitus results from T cell-mediated destruction of insulin-producing beta cells in the pancreas, leading to insufficient insulin production and impaired glucose regulation.

Systemic lupus erythematosus (SLE) and rheumatoid arthritis are systemic autoimmune diseases linked to type III hypersensitivity reactions, which involve immune complex formation. In SLE, autoantibodies bind to various autoantigens, including nuclear components like DNA, forming immune complexes that deposit throughout the body and cause widespread organ damage. Rheumatoid arthritis is characterized by the accumulation of immune complexes in joints, triggering severe inflammation and pain. It is important to distinguish rheumatoid arthritis from osteoarthritis, the latter being a degenerative joint disease caused by mechanical wear and tear rather than immune dysfunction.

Currently, there are no cures for autoimmune diseases; treatments focus on managing symptoms and slowing disease progression. This highlights the ongoing need for research to better understand the underlying mechanisms of autoimmune disorders and develop more effective therapies.

Autoimmune Diseases Example 1

Autoimmune diseases are classified based on the type of hypersensitivity reaction involved and the specific tissues targeted by the immune system. Rheumatoid arthritis is a classic example of a type III hypersensitivity autoimmune disorder, where immune complexes—combinations of antigens and antibodies—are deposited in the joints, leading to inflammation and joint damage. This immune complex deposition triggers an inflammatory response that causes the characteristic symptoms of rheumatoid arthritis.

Graves' disease represents a non-cytotoxic type II hypersensitivity reaction. In this condition, autoantibodies mimic thyroid-stimulating hormone (TSH) and bind to thyroid cells, causing overstimulation of the thyroid gland. This results in excessive production of thyroid hormones, leading to hyperthyroidism and its associated symptoms.

Multiple sclerosis (MS) is an autoimmune disease driven by a type IV hypersensitivity reaction, where T cells, antibodies, and macrophages mistakenly attack the myelin sheath surrounding nerve fibers. This demyelination disrupts nerve signal transmission, causing neurological symptoms such as muscle weakness, coordination problems, and sensory disturbances.

Type 1 diabetes mellitus is also a type IV hypersensitivity autoimmune disorder characterized by the immune system's T cells targeting and destroying insulin-producing beta cells in the pancreas. The loss of these cells leads to insufficient insulin production, resulting in elevated blood glucose levels and the clinical manifestations of diabetes.

Understanding these autoimmune diseases involves recognizing the specific immune mechanisms—such as immune complex deposition, antibody-mediated receptor stimulation, and T cell-mediated cytotoxicity—that underlie tissue damage. This knowledge is essential for diagnosing, managing, and developing targeted therapies for autoimmune conditions.

_________ is an organ-specific autoimmune disease where the immune system damages the protective covering of the nerve cells (myelin sheath) in the body. This disease results in pain, fatigue, loss of coordination, and other adverse symptoms over a patient’s lifetime.

• A. Graves’ Disease.
• B. Rheumatoid arthritis.
• C. Multiple sclerosis.
• D. Addison’s disease.

Answer: (A)

Which of the following statements about lupus erythematosus & multiple sclerosis is true?

• A. Lupus is an organ-specific autoimmune disease, multiple sclerosis is systemic.
• B. They’re both autoimmune diseases, but lupus is a type III hypersensitivity while multiple sclerosis is a type IV hypersensitivity.
• C. Lupus is caused by T cell-mediated immune responses, multiple sclerosis is due to immune complexes.
• D. Lupus is a cell-specific autoimmune disease that only damages erythrocytes, multiple sclerosis only affects nerve cells

Answer: (B)

Factors Contributing to Autoimmune Diseases

Autoimmune diseases arise when the immune system mistakenly attacks the body's own tissues, and while the exact causes remain not fully understood, three primary factors contribute significantly to their development. Genetics play a crucial role, as many autoimmune diseases exhibit a strong family history, indicating a hereditary component, although the specific genes involved have yet to be precisely identified. Environmental factors also influence the onset of autoimmune conditions; these include smoking, certain medications, dietary elements, and infections caused by pathogens. Some pathogens possess antigens that closely resemble the body's own molecules, a phenomenon known as molecular mimicry. For instance, the Epstein-Barr virus shares structural similarities with myelin, the protective sheath around nerve fibers. An immune response targeting this virus can inadvertently attack myelin, contributing to diseases like multiple sclerosis.

Another critical factor is immune regulation defects. Normally, autoreactive T cells that could attack self-tissues are eliminated during their development in the thymus. However, if this process malfunctions, these self-reactive T cells may escape into circulation, promoting autoimmune reactions. Despite understanding this mechanism, the precise reasons behind such immune regulation failures remain unclear. Interestingly, autoimmune diseases disproportionately affect women, accounting for approximately 80% of cases. Although several hypotheses attempt to explain this gender disparity, definitive explanations are still lacking, highlighting the need for ongoing research.

Understanding these factors—genetics, environmental triggers, and immune regulation defects—provides a foundation for exploring autoimmune diseases. This knowledge is essential for developing targeted therapies and improving diagnostic methods, ultimately advancing patient care in immunology.

An individual can develop an autoimmune disease for a variety of reasons. Which of the following examples is NOT a way that someone could develop an autoimmune disease?

• A. A person’s exposure to environmental toxins can trigger the development of or exacerbate systemic lupus.
• B. A son inherits genes from his mother which are strongly associated with developing Graves’ disease.
• C. Someone gets doses of too many different vaccines & their immune system begins attacking self-cells.
• D. T cells that mistakenly attack self-antigens are not destroyed in the thymus.
• E. All of the above are ways that someone could develop an autoimmune disorder.

Answer: (C)

Here’s what students ask on this topic:

What are autoimmune diseases and how do they affect the immune system?

Autoimmune diseases are conditions where the immune system mistakenly attacks the body's own tissues instead of foreign pathogens. Normally, the immune system defends against harmful invaders, but in autoimmune diseases, it produces autoantibodies or autoreactive T cells that target self antigens. This misdirected immune response can damage specific organs or affect multiple systems throughout the body. These diseases arise due to defects in humoral immunity (involving plasma cells producing autoantibodies) or cell-mediated immunity (involving autoreactive T cells killing self cells). Collectively, autoimmune diseases affect about 5-10% of the population, highlighting their significance in human health.

What are some common examples of autoimmune diseases and their mechanisms?

Common autoimmune diseases include Graves' disease, myasthenia gravis, multiple sclerosis (MS), type 1 diabetes mellitus, systemic lupus erythematosus (SLE), and rheumatoid arthritis. Graves' disease involves autoantibodies overstimulating thyroid hormone production. Myasthenia gravis features autoantibodies blocking receptors at neuromuscular junctions, reducing muscle activity. MS and type 1 diabetes are T cell-mediated diseases where autoreactive T cells attack myelin in nerves and insulin-producing pancreatic cells, respectively. SLE and rheumatoid arthritis involve immune complexes formed by autoantibodies binding self antigens, causing systemic inflammation and joint damage. These diseases illustrate how both humoral and cell-mediated immunity can contribute to autoimmune pathology.

What factors contribute to the development of autoimmune diseases?

Autoimmune diseases develop due to a combination of genetic, environmental, and immune regulation factors. Genetics play a role as some diseases show family history, though specific genes are not fully identified. Environmental triggers include smoking, certain drugs, diet, and infections; some pathogens mimic host antigens, leading to cross-reactive immune responses. For example, Epstein-Barr virus shares similarities with myelin, potentially triggering multiple sclerosis. Immune regulation defects, such as failure to eliminate autoreactive T cells in the thymus, also contribute. Notably, about 80% of autoimmune cases occur in women, though the reasons remain unclear, indicating ongoing research is needed.

How do autoimmune diseases differ between organ-specific and systemic types?

Autoimmune diseases can be classified as organ-specific or systemic based on the extent of their impact. Organ-specific autoimmune diseases target a single organ or tissue, causing localized damage. Examples include Graves' disease affecting the thyroid and type 1 diabetes mellitus targeting pancreatic cells. Systemic autoimmune diseases affect multiple organs or systems throughout the body, leading to widespread symptoms. Examples include systemic lupus erythematosus (SLE), which involves immune complexes damaging various organs, and rheumatoid arthritis, which primarily affects joints but can have systemic effects. Understanding this distinction helps in diagnosis and treatment planning.

Why are autoimmune diseases more common in women than men?

Approximately 80% of autoimmune disease cases occur in women, but the exact reasons are not fully understood. Several hypotheses suggest hormonal differences, such as the effects of estrogen on immune function, may influence susceptibility. Women’s immune systems tend to be more reactive, which can increase the risk of autoimmunity. Genetic factors linked to the X chromosome, which women have two copies of, might also play a role. Additionally, environmental and epigenetic factors could contribute. Despite these theories, more research is needed to clarify why women are disproportionately affected by autoimmune diseases.

Are there cures for autoimmune diseases, and how are they currently managed?

Currently, there are no cures for autoimmune diseases. Treatments focus on managing symptoms and controlling the immune system's abnormal activity. Therapies may include immunosuppressive drugs, corticosteroids, and biologics that target specific immune pathways. These treatments aim to reduce inflammation, prevent tissue damage, and improve quality of life. Because autoimmune diseases vary widely in their mechanisms and severity, treatment plans are often personalized. Ongoing research seeks to better understand these diseases to develop more effective and potentially curative therapies in the future.