Autoimmune Disease- Definition, Types, and Examples

An autoimmune disease is a condition in which the immune system mistakenly attacks the body`s own cells and tissues, causing inflammation and damage. The immune system normally protects the body from foreign invaders, such as bacteria and viruses, by producing antibodies and other immune cells that recognize and eliminate them. However, sometimes the immune system fails to distinguish between self and non-self, and launches an inappropriate response against its own tissues. This can result in various symptoms and complications, depending on the type and severity of the autoimmune disease.

There are more than 80 different types of autoimmune diseases, affecting various organs and systems of the body. Some of the most common ones are:

• Type 1 diabetes: a condition in which the immune system destroys the insulin-producing cells of the pancreas, leading to high blood sugar levels and complications such as kidney damage, nerve damage, and blindness.
• Rheumatoid arthritis: a condition in which the immune system attacks the joints, causing pain, swelling, stiffness, and deformity.
• Multiple sclerosis: a condition in which the immune system attacks the protective coating of the nerve fibers in the brain and spinal cord, causing problems with vision, movement, balance, and coordination.
• Psoriasis: a condition in which the immune system causes the skin cells to grow too fast, resulting in red, scaly patches that can itch and bleed.
• Lupus: a condition in which the immune system affects various parts of the body, such as the skin, joints, kidneys, blood cells, heart, and lungs, causing symptoms such as rash, fatigue, fever, and joint pain.

The exact causes of autoimmune diseases are not fully understood, but they are likely influenced by a combination of genetic and environmental factors. Some people may inherit genes that make them more susceptible to developing an autoimmune disease, while others may be triggered by infections, stress, hormones, or other factors. Autoimmune diseases are more common in women than in men, and they often run in families.

Autoimmune diseases can be diagnosed by various tests that measure the levels of antibodies or other immune markers in the blood or other fluids. Treatment options vary depending on the type and severity of the autoimmune disease, but they generally aim to reduce inflammation and suppress or modulate the immune system. Some common treatments include anti-inflammatory drugs, corticosteroids, immunosuppressants, biologics (drugs derived from living organisms), and stem cell transplantation.

Autoimmune diseases can have a significant impact on the quality of life of those affected by them. They can cause chronic pain, disability, organ damage, and increased risk of infections and cancers. They can also affect mental health by causing anxiety, depression, and emotional distress. Therefore, it is important to seek medical attention if you experience any signs or symptoms of an autoimmune disease. Early diagnosis and treatment can help prevent or delay complications and improve your well-being.

A hypersensitivity reaction is an abnormal immune response that causes tissue damage or disease. It occurs when the immune system recognizes a foreign substance (antigen) as harmful and mounts an exaggerated or inappropriate response against it. The antigen may be a microbe, a drug, a food, a pollen, or even a self-antigen in some cases.

There are four types of hypersensitivity reactions, classified according to the type of immune cells and molecules involved and the mechanism of tissue damage. They are:

• Type I hypersensitivity: This is also called immediate or anaphylactic hypersensitivity. It is mediated by IgE antibodies that bind to mast cells and basophils. When these cells encounter the antigen, they release histamine and other inflammatory mediators that cause vasodilation, smooth muscle contraction, increased vascular permeability, and mucus secretion. This leads to symptoms such as itching, hives, sneezing, wheezing, swelling, and anaphylactic shock in severe cases. Examples of type I hypersensitivity are allergic rhinitis, asthma, food allergies, and bee sting allergies.
• Type II hypersensitivity: This is also called antibody-dependent or cytotoxic hypersensitivity. It is mediated by IgG or IgM antibodies that bind to cell surface antigens or extracellular matrix components. These antibodies activate the complement system or recruit phagocytes and natural killer cells that destroy the target cells by lysis or phagocytosis. This leads to symptoms such as hemolysis, thrombocytopenia, neutropenia, and tissue damage. Examples of type II hypersensitivity are autoimmune hemolytic anemia, Goodpasture`s syndrome, Graves` disease, and myasthenia gravis.
• Type III hypersensitivity: This is also called immune complex-mediated hypersensitivity. It is mediated by IgG or IgM antibodies that form complexes with soluble antigens in the circulation or in tissues. These complexes deposit in various sites such as blood vessels, joints, kidneys, and skin, where they activate the complement system and trigger inflammation. This leads to symptoms such as vasculitis, arthritis, glomerulonephritis, and skin lesions. Examples of type III hypersensitivity are systemic lupus erythematosus (SLE), rheumatoid arthritis, serum sickness, and Arthus reaction.
• Type IV hypersensitivity: This is also called cell-mediated or delayed-type hypersensitivity. It is mediated by T cells that recognize antigens presented by antigen-presenting cells (APCs) such as macrophages or dendritic cells. These T cells secrete cytokines that recruit and activate other immune cells such as macrophages, eosinophils, and cytotoxic T cells that cause tissue damage by inflammation or direct killing. This leads to symptoms such as granuloma formation, contact dermatitis, tuberculin reaction, and transplant rejection. Examples of type IV hypersensitivity are tuberculosis, leprosy, poison ivy rash, type I diabetes mellitus (IDDM), and multiple sclerosis.

Hypersensitivity reactions can be triggered by various factors such as infections, drugs, vaccines, environmental agents, or genetic predisposition. They can be acute or chronic depending on the duration and severity of the immune response. They can also be localized or systemic depending on the extent of tissue involvement.

Hypersensitivity reactions are important causes of morbidity and mortality worldwide. They can affect any organ or system of the body and cause various clinical manifestations ranging from mild to life-threatening. They can also complicate the diagnosis and treatment of other diseases.

Hypersensitivity reactions can be prevented or treated by avoiding or removing the triggering antigen if possible; using drugs that suppress or modulate the immune response such as antihistamines, corticosteroids, immunosuppressants; using desensitization therapy that induces tolerance to the antigen by repeated exposure; using immunotherapy that enhances the protective immunity against the antigen by vaccination; or using gene therapy that corrects the underlying genetic defect that causes the abnormal immune response.

Hypersensitivity reactions are examples of how the immune system can sometimes go wrong and harm the body instead of protecting it. They illustrate the need for a balance between immunity and tolerance in maintaining health and preventing disease.

As mentioned earlier, hypersensitivity reactions are immunological responses that cause tissue damage. They are classified into four types based on the type of antigen, antibody, and effector mechanism involved. Here is a brief overview of each type:

• Type I hypersensitivity is also known as immediate hypersensitivity or allergy. It is mediated by IgE antibodies that bind to mast cells and basophils. When these cells encounter an allergen (such as pollen, dust mites, or food), they release histamine and other inflammatory mediators that cause symptoms such as itching, sneezing, wheezing, and anaphylaxis. Examples of type I hypersensitivity diseases are allergic rhinitis, asthma, urticaria, and food allergies.

• Type II hypersensitivity is also known as cytotoxic hypersensitivity or antibody-dependent cellular cytotoxicity (ADCC). It is mediated by IgG or IgM antibodies that bind to cell-surface or matrix antigens. These antibodies activate the complement system and/or recruit natural killer (NK) cells, macrophages, or neutrophils that destroy the target cells. Examples of type II hypersensitivity diseases are hemolytic anemia, transfusion reactions, autoimmune hemolytic anemia, and Graves` disease.

• Type III hypersensitivity is also known as immune complex-mediated hypersensitivity. It is mediated by IgG or IgM antibodies that form immune complexes with soluble antigens. These complexes deposit in various tissues and trigger the complement system and/or recruit inflammatory cells that cause tissue damage. Examples of type III hypersensitivity diseases are serum sickness, Arthus reaction, glomerulonephritis, and systemic lupus erythematosus (SLE).

• Type IV hypersensitivity is also known as delayed-type hypersensitivity (DTH) or cell-mediated hypersensitivity. It is mediated by T cells, either helper T cells (TH1 or TH2) or cytotoxic T cells (CTL). These T cells recognize antigens presented by antigen-presenting cells (APCs) and secrete cytokines that activate macrophages, eosinophils, or CTLs that cause tissue damage. Examples of type IV hypersensitivity diseases are contact dermatitis, tuberculin reaction, granulomatous inflammation, and type I diabetes mellitus (IDDM).

These four types of hypersensitivity reactions can be involved in different autoimmune diseases, depending on the nature of the self-antigens and the immune effector mechanisms that cause tissue injury. In the next section, we will discuss some examples of organ-specific and systemic autoimmune diseases and how they relate to these types of hypersensitivity reactions.

Autoimmune diseases can be classified into two broad categories: organ-specific and systemic. Organ-specific autoimmune diseases are those in which the immune system targets a specific organ or tissue of the body, such as the thyroid gland, the pancreas, or the eye. Systemic autoimmune diseases are those in which the immune system attacks multiple organs or tissues throughout the body, such as the skin, the joints, or the blood vessels.

The distinction between organ-specific and systemic autoimmune diseases is not always clear-cut, as some diseases may have features of both categories. For example, rheumatoid arthritis is considered a systemic disease because it affects the joints and other tissues, but it also involves autoantibodies against specific antigens expressed on synovial cells. Similarly, multiple sclerosis is considered an organ-specific disease because it affects the central nervous system, but it also involves T cells that react to various myelin antigens.

The difference between organ-specific and systemic autoimmune diseases may reflect the nature and location of the self-antigens involved. Organ-specific autoimmune diseases may be caused by self-antigens that are unique to a particular organ or tissue, or that are sequestered from the immune system during development. For example, thyroid peroxidase is an enzyme that is only expressed in thyroid follicular cells, and is a target of autoantibodies in Hashimoto`s thyroiditis and Graves` disease. Similarly, insulin is a hormone that is only produced by pancreatic beta cells, and is a target of autoantibodies and T cells in type I diabetes.

Systemic autoimmune diseases may be caused by self-antigens that are widely distributed throughout the body, or that are exposed to the immune system under certain conditions. For example, DNA and histones are components of chromatin that are present in all nucleated cells, and are targets of autoantibodies in systemic lupus erythematosus. Similarly, heat-shock proteins are molecules that are induced by stress and infection in various cells, and are targets of T cells in some forms of arthritis.

The diagnosis and treatment of autoimmune diseases may depend on whether they are organ-specific or systemic. Organ-specific autoimmune diseases may be easier to diagnose because they often have characteristic signs and symptoms related to the affected organ. For example, hypothyroidism or hyperthyroidism can be detected by measuring thyroid hormone levels in the blood. Organ-specific autoimmune diseases may also be easier to treat because they can be targeted by therapies that modulate or replace the function of the damaged organ. For example, type I diabetes can be treated by insulin injections or transplantation of pancreatic islets.

Systemic autoimmune diseases may be harder to diagnose because they often have nonspecific signs and symptoms that affect various organs and tissues. For example, fatigue, fever, rash, and joint pain can be caused by many different conditions besides systemic lupus erythematosus. Systemic autoimmune diseases may also be harder to treat because they require therapies that suppress or modulate the overall immune response. For example, corticosteroids, immunosuppressants, and biologics are drugs that can reduce inflammation and autoimmunity in systemic diseases.

Organ-specific and systemic autoimmune diseases are both examples of how the immune system can malfunction and cause harm to the body. By understanding the differences between these two categories of disease, we can better diagnose and treat patients with autoimmune disorders.

Organ-specific autoimmune diseases are those in which the immune system targets a specific organ or tissue and causes damage or dysfunction. The exact mechanisms of organ-specific autoimmunity are not fully understood, but they may involve genetic susceptibility, environmental triggers, molecular mimicry, epitope spreading, and loss of tolerance. Some of the most common and well-studied organ-specific autoimmune diseases are:

• Hashimoto`s thyroiditis: This is a chronic inflammatory condition of the thyroid gland, in which autoantibodies and T cells attack the thyroid follicular cells and impair their ability to produce thyroid hormones. This leads to hypothyroidism, or low levels of thyroid hormones in the blood. Symptoms may include fatigue, weight gain, cold intolerance, dry skin, hair loss, constipation, and depression. Hashimoto`s thyroiditis is more common in women than in men and may be associated with other autoimmune diseases such as celiac disease and type 1 diabetes.
• Graves` disease: This is another autoimmune disorder of the thyroid gland, but in this case, the immune system stimulates the thyroid follicular cells to produce excessive amounts of thyroid hormones. This leads to hyperthyroidism, or high levels of thyroid hormones in the blood. Symptoms may include nervousness, weight loss, heat intolerance, palpitations, tremors, exophthalmos (bulging eyes), and goiter (enlarged thyroid gland). Graves` disease is also more common in women than in men and may be triggered by stress, infection, or pregnancy.
• Type 1 diabetes mellitus (T1DM): This is a metabolic disorder in which the immune system destroys the insulin-producing beta cells of the pancreatic islets. Insulin is a hormone that regulates the uptake of glucose from the blood into the cells for energy production. Without insulin, glucose accumulates in the blood and causes hyperglycemia (high blood sugar levels). Symptoms may include increased thirst, urination, hunger, weight loss, fatigue, blurred vision, and ketoacidosis (a life-threatening condition caused by the breakdown of fat for energy). T1DM usually develops in childhood or adolescence and requires lifelong insulin injections to manage blood glucose levels. T1DM may be associated with other autoimmune diseases such as celiac disease and autoimmune thyroiditis.
• Multiple sclerosis (MS): This is a chronic inflammatory disease of the central nervous system (CNS), in which the immune system attacks the myelin sheath that surrounds and protects the nerve fibers. Myelin is a fatty substance that enables fast and efficient transmission of nerve impulses. Damage to myelin causes disruption of nerve communication and leads to various neurological symptoms such as numbness, tingling, weakness, spasticity, vision problems, cognitive impairment, fatigue, and depression. MS is more common in women than in men and may have a relapsing-remitting or a progressive course. The exact cause of MS is unknown, but it may involve genetic predisposition, environmental factors such as viral infections or vitamin D deficiency, and molecular mimicry between myelin antigens and foreign antigens.
• Myasthenia gravis (MG): This is a neuromuscular disorder in which the immune system produces autoantibodies that block or destroy the acetylcholine receptors on the muscle cells. Acetylcholine is a neurotransmitter that enables muscle contraction when it binds to its receptors. Without acetylcholine receptors, muscle cells cannot respond to nerve signals and become weak and fatigued. Symptoms may include drooping eyelids (ptosis), double vision (diplopia), difficulty swallowing (dysphagia), difficulty speaking (dysarthria), difficulty breathing (dyspnea), and generalized weakness that worsens with activity. MG may affect any voluntary muscle group but usually starts with the muscles of the eyes and face. MG may be associated with other autoimmune diseases such as thymoma (a tumor of the thymus gland) or rheumatoid arthritis.

These are just some examples of organ-specific autoimmune diseases. There are many others that affect different organs or tissues such as the liver (autoimmune hepatitis), the stomach (pernicious anemia), the skin (vitiligo), the joints (rheumatoid arthritis), or the blood vessels (vasculitis). Organ-specific autoimmune diseases can have a significant impact on the quality of life and health outcomes of affected individuals. Therefore, early diagnosis and appropriate treatment are essential to prevent or reduce complications and improve prognosis.

Examples of Systemic Autoimmune Diseases

Systemic autoimmune diseases are characterized by the involvement of multiple organs or tissues in the immune-mediated inflammatory process. Unlike organ-specific autoimmune diseases, which target a single organ or tissue type, systemic autoimmune diseases can affect any part of the body. Some of the most common and well-known examples of systemic autoimmune diseases are:

• Systemic lupus erythematosus (SLE): SLE is a chronic inflammatory disease that can affect the skin, joints, kidneys, blood cells, heart, lungs, and brain. The hallmark feature of SLE is the production of autoantibodies against nuclear antigens, such as DNA, histones, and ribonucleoproteins. These autoantibodies form immune complexes that deposit in various tissues and trigger inflammation and tissue damage. The symptoms of SLE vary widely depending on the organs involved and the severity of the disease. Some common symptoms include rash, arthritis, fatigue, fever, anemia, nephritis, and neurological disorders.

• Rheumatoid arthritis (RA): RA is a chronic inflammatory disease that primarily affects the synovial joints, causing pain, swelling, stiffness, and deformity. RA is also associated with systemic manifestations, such as rheumatoid nodules, vasculitis, lung fibrosis, and cardiovascular complications. The main cause of RA is the activation of auto-reactive T cells and B cells that produce inflammatory cytokines and autoantibodies against joint antigens, such as citrullinated proteins and rheumatoid factor. These immune mediators induce synovitis and cartilage and bone erosion.

• Sjögren`s syndrome: Sjögren`s syndrome is a chronic inflammatory disease that mainly affects the exocrine glands, such as the salivary and lacrimal glands, resulting in dry mouth and dry eyes. Sjögren`s syndrome can also affect other organs, such as the lungs, kidneys, liver, pancreas, nervous system, and blood vessels. The pathogenesis of Sjögren`s syndrome involves the infiltration of lymphocytes into the affected glands and the production of autoantibodies against various antigens, such as Ro/SSA and La/SSB. These immune mechanisms impair the function and secretion of the glands.

• Scleroderma: Scleroderma is a chronic inflammatory disease that causes fibrosis and thickening of the skin and internal organs. Scleroderma can be classified into two main types: localized scleroderma, which affects only the skin; and systemic scleroderma, which affects multiple organs, such as the lungs, heart, kidneys, gastrointestinal tract, and blood vessels. The etiology of scleroderma is not fully understood, but it involves the activation of fibroblasts by cytokines and growth factors produced by immune cells and endothelial cells. The fibroblasts produce excessive amounts of collagen and other extracellular matrix components that accumulate in the tissues and impair their function.

These are some of the most common examples of systemic autoimmune diseases. There are many other types of systemic autoimmune diseases that affect different organs or tissues in various ways. Some examples are mixed connective tissue disease (MCTD), polyarteritis nodosa (PAN), polymyositis (PM), dermatomyositis (DM), vasculitis syndromes (e.g., Wegener`s granulomatosis), antiphospholipid syndrome (APS), autoimmune hepatitis (AIH), primary biliary cirrhosis (PBC), autoimmune hemolytic anemia (AIHA), immune thrombocytopenic purpura (ITP), and autoimmune thyroiditis (AIT).

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