In this article, I briefly describe organ-specific autoimmune diseases.
The term “autoimmunity” defines the failure of a person’s immune system to recognize its cells as self. Thus, the immune system mounts an immune response against its healthy cells. Disease resulting from this type of immune response is known as autoimmune disease. Self-components are recognized by immune-stimulatory lymphocytes, which cause cellular lysis along with an inflammatory response in the affected organ.
Some autoimmune diseases precisely target some organs, and that’s why the effects are limited to that organ. These are categorized as systemic, as they can affect multiple systems in the body. Some organ-specific autoimmune diseases are discussed below.
Organ-specific autoimmune diseases
Type 1 Diabetes
The disease, also known as insulin-dependent diabetes mellitus, is less common than type 2 diabetes and affects mainly children. It is a chronic condition where the pancreas secretes no insulin or very little in amount. Though anyone can get affected with type 1 diabetes, it is quite common in children and adolescents. In the absence of insulin, blood sugar can’t find its way into cells and accumulate in the bloodstream. High blood sugar begins to create many complications of diabetes.
Insulin is produced by pancreatic beta cells, which suffer an autoimmune attack. Thus, these cells produce very little insulin or no insulin at all and ultimately raise blood sugar levels. The islets of Langerhans, a collection of endocrine tissue located in the pancreas, regulate glucose levels. When it gets inflamed, it goes through infiltration of T and B lymphocytes, macrophages, and dendritic cells.
The condition known as insulitis leads to a cell-mediated DTH response, causing the release of cytokines and the production of autoantibodies. The release of cytokines by the DTH response and the lytic enzymes released from the activated macrophages cause the destruction of beta-cells in the pancreas.
Autoantibodies destroy beta cells by either antibody-mediated complement lysis or antibody-dependent cell-mediated cytotoxicity.
The anomaly in glucose metabolism associated with type 1 diabetes results in a serious metabolic condition known as ketoacidosis. In this condition, ketone (a breakdown product of fat) accumulates and ultimately results in increased urine production. The final stages of this disease, can be marked by atherosclerotic vascular lesions, renal failure, and blindness. Lack of treatment may cause fatal conditions. Type 1 diabetes is commonly treated with the administration of insulin regularly every day. If the disease remains undetected, it can lead to irreparable loss of pancreatic tissue.
Experiment with Non-obese diabetic mouse (NOD)
The non-obese diabetic mouse is the best experimental animal that develops a form of diabetes resembling human diabetes. Thus, it can be compared with other complications of the disease. This form of the disease also involves the destruction of pancreatic beta cells by the lymphocytic infiltration of the pancreas. This disorder also has a strong association with certain MHC alleles.
Bone marrow cells arbitrate the disease as normal mice develop the disease by getting an injection of bone marrow cells from NOD mice. Healthy NOD mice, when reconstituted with bone marrow cells from MHC-matched normal mice, can get escaped from developing the disease. In an experiment, when germ germ-free environment is provided to NOD mice, a greater tendency of developing type 1 diabetes is noticed in comparison to staying in a normal house environment, which suggests that autoimmune diseases, are hindered by a diverse flora.
The disease affects more women in comparison to men during their middle age. A person suffering from Hashimoto’s thyroiditis produces auto-antibodies and sensitized TH1 cells, specific for thyroid antigens.
Antibodies are formed against several thyroid proteins like thyroglobulin and thyroid peroxidase. The uptake of iodine is hindered by the binding of auto-antibodies to these proteins. The hindrance of iodine uptake results in the low functioning of the thyroid gland and the development of hypothyroidism.
A delayed type hypersensitivity response is developed, which causes severe infiltration of lymphocytes, follicles, and germinal centers into the thyroid gland. The subsequent inflammatory response causes a marked enlargement of the thyroid gland known as goiter. Antibodies reacting against thyroid-specific proteins cause local inflammation, and the formation of goiter is a physiological response to it. This response lowers the function of the thyroid gland, which ultimately results in fatigue, laziness, and unexplained weight gain.
The thyroid gland secretes the hormone thyroxine. The daily administration of the hormone brings relief from the symptoms and lets people lead a normal life.
It is a chronic auto-immune disorder, which involves the destruction of communication between nerves and muscles. An individual suffering from this disease produces auto-antibodies that bind with the acetylcholine receptors on the motor end plates of muscles. The binding of antibodies (mainly IgG1 and IgG3) blocks the usual binding of acetylcholine with its receptor. Thus, this induces complement-mediated lysis of the cells. It results in the gradual weakening of the skeletal muscles.
The antibodies destroy the cells bearing acetylcholine receptors. The disease myasthenia gravis affects the voluntary muscles of the body, controlling the eyes, mouth, throat, and limbs.
The early symptoms of the disease include drooping of eyelids and double vision, difficulties in talking and walking, and inability to retract the corners of the mouth. If left untreated, then this leads to subsequent weakening of the muscles. This eventually results in problems with movement and severe impairment in eating. It is difficult to diagnose the disease early as it is hard to distinguish it from other neurological disorders.
However, with proper treatment, this disease can be controlled, and the affected individual can lead a normal life. Myasthenia gravis is generally treated with medications known as acetylcholinesterase inhibitors, such as neostigmine and pyridostigmine. Some immunosuppressants also can be used to control the disease. The disease primarily affects women under the age of forty and men over the age of sixty.
In general, children do not get affected by this disease. Pregnant women having myasthenia gravis begin to worsen their symptoms in the first trimester of pregnancy. Immunosuppressive therapy should be maintained throughout pregnancy as this inhibits neonatal muscle weakness and also controls the disease.
Some autoimmune diseases precisely target some organs, so the effects are limited to that organ only. Some organ-specific autoimmune diseases are type-1 diabetes, Hashimoto’s thyroiditis, and myasthenia gravis.
Type-1 diabetes is a chronic condition where the pancreas secretes no insulin or very little in amount. Insulin is produced by Pancreatic beta cells, which undergo an autoimmune attack. Thus, these cells are unable to produce the required insulin, which raises the blood sugar levels. The anomaly in glucose metabolism associated with type 1 diabetes, results in a serious metabolic condition known as ketoacidosis. Type 1 diabetes is commonly treated with the administration of insulin regularly every day.
When a person suffers from Hashimoto’s thyroiditis, then autoantibodies and sensitized TH1 cells are produced, which are specific for thyroid antigens. The uptake of iodine, is hindered by the binding of autoantibodies to the proteins, thyroglobulin, and thyroid peroxidase. The hindrance of iodine uptake results in the low functioning of the thyroid gland and the development of hypothyroidism. The daily administration of the hormone thyroxine brings relief from the symptoms and lets people lead a normal life.
Myasthenia gravis is a chronic auto-immune disorder, which involves the destruction of communication between nerves and muscles. An individual suffering from this disease produces autoantibodies that bind with the acetylcholine receptors on the motor end plates of muscles. Myasthenia gravis is generally treated with medications known as acetylcholinesterase inhibitors, such as neostigmine and pyridostigmine.
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I, Swagatika Sahu (author of this website), have done my master’s in Biotechnology. I have around twelve years of experience in writing and believe that writing is a great way to share knowledge. I hope the articles on the website will help users in enhancing their intellect in Biotechnology.