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What are autoantibodies

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    What are autoantibodies?


    What are they?
    Autoantibodies are a group of antibodies (immune proteins) that mistakenly target and damage specific tissues or organs of the body. One or more autoantibodies may be produced by a person’s immune system when it fails to distinguish between “self” and “non-self" proteins. Usually the immune system is able to discriminate by recognizing foreign substances (“non-self”) and ignoring the body’s own cells ("self"), yet not overreact to non-threatening substances such as foods, dust and pollen, or beneficial microorganisms. It creates antibodies only when it perceives what it has been exposed to as a threat ("non-self"). When the immune system ceases to recognize one or more of the body’s normal constituents as “self”, it may produce autoantibodies that attack its own cells, tissues, and/or organs, causing inflammation and damage. The causes of this inappropriate action are varied and are not well understood, often resulting in a chronic autoimmune disorder. While there is not a direct link, it is thought that many cases of autoantibody production are due to a genetic predisposition combined with an environmental trigger (such as a viral illness or a prolonged exposure to certain toxic chemicals). Some families have been shown to have a high prevalence of autoimmune conditions; however, individual family members may have different autoimmune disorders or may never develop an autoimmune condition. Researchers believe that there may also be a hormonal component to the cause as many of the autoimmune conditions are more common in women of childbearing age.

    The type of autoimmune disorder or disease that occurs and the amount of destruction done to the body depends on which systems or organs are targeted by the autoantibodies. Disorders caused by autoantibodies that primarily affect a single organ, such as the thyroid in Graves’ disease or Hashimoto’s thyroiditis, are often the easiest to diagnose as they frequently present with organ-related symptoms.

    Disorders due to systemic autoantibodies (affects multiple organs or systems) can be much more elusive. Although the associated autoimmune disorders are rare, the signs and symptoms they cause are relatively common and may include: arthritis-type joint pain, fatigue, fever, rashes, cold or allergy-type symptoms, weight loss, and muscular weakness. Additional complications may include vasculitis (inflammation of blood vessels) and anemia. Signs and symptoms will vary from person to person. They can vary over time and/or with organ involvement, often tapering off and then flaring up unexpectedly. To complicate the situation, some may have more than one autoantibody, have more than one autoimmune disorder, and/or have an autoimmune disorder without a detectable level of an autoantibody. This may make it difficult for the doctor to identify the prime cause and arrive at a diagnosis.

    The role of apoptosis in autoimmune thyroid disorders and thyroid cancer

    Jen-Der Lin, professor of internal medicine

    Division of Endocrinology and Metabolism, Department of Internal Medicine, Chang Gung Memorial Hospital, Chang Gung University, 5 Fu-Shin Street, Kweishan County, Taoyuan Hsien, Taiwan, Republic of China

    Apoptosis, or programmed cell death, is an active process of self destruction that requires the activation of a genetic programme that may lead to changes in cell morphology, DNA fragmentation, and protein cross linking Apoptosis can be triggered in severalways and involves many cellular functions. The mechanism provides protection from the possible consequences of uncontrolled cell proliferation, which could lead to neoplasia. Cell death is a factor in the pathogenesis of several diseases, including autoimmunedisorders, cancer, AIDS, and neurodegenerative diseases. Regulationof apoptosis in cells undergoing proliferation may be the key to reversing the natural progression of these disorders. Apoptosis involves the sequential activation of a series of caspases, whichare proteolytic enzymes that degrade a number of death substrates. Caspase is activated by two pathways---the mitochondrial pathway and the death receptor pathway---and thereby may trigger nuclear enzymes to degrade chromosomal DNA and alter mitochondrial function. Specific pathways and non-specific signals (such as cytotoxic drugs and radiation) may activate caspase. The most common ofthese pathways involves death receptors that have structures belongingto the tumour necrosis factor (TNF) receptor superfamily of proteins. Interaction of tumour necrosis factor with this receptor can induce cell death by the activation of various kinase enzymes that act as secondary messengers within the cell, Another member of this family, Fas antigen, and its ligand (FasL), are molecules used by immune effector cells to kill targets. 

     

     

     

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