Related Experiment Video
Updated: May 4, 2026

09:15
Electrochemiluminescence Assays for Human Islet Autoantibodies
Published on: March 23, 2018
15.9K
Human monoclonal autoantibodies that react with both pancreatic islets and thyroid
The Journal of Clinical Investigation
|May 1, 1986
Summary
Researchers identified common human autoantibodies targeting both the pancreas and thyroid. This discovery utilized Epstein-Barr virus transformation of lymphocytes and enzyme-linked immunosorbent assay screening.
Area of Science:
- Immunology
- Endocrinology
- Cell Biology
Background:
- Autoantibodies play a role in autoimmune diseases affecting endocrine glands.
- The presence and specificity of autoantibodies in the general population are not fully understood.
Purpose of the Study:
- To identify and characterize monoclonal autoantibodies reacting with human pancreatic islets.
- To investigate the prevalence of lymphocytes producing autoantibodies against both pancreatic islets and thyroid.
Main Methods:
- Human peripheral blood lymphocytes were transformed using Epstein-Barr virus.
- Rat insulinoma cells were screened using an enzyme-linked immunosorbent assay (ELISA) to detect autoantibody reactivity.
- Isolated monoclonal autoantibodies were cloned and further tested for reactivity against human thyroid tissue.
Main Results:
- Six monoclonal autoantibodies that react with human pancreatic islets were successfully isolated and cloned.
- All six identified autoantibodies also demonstrated reactivity with human thyroid tissue.
- These findings suggest a common B cell repertoire capable of producing autoantibodies against both organs.
Conclusions:
- Autoantibodies targeting both the pancreas and thyroid are common in the human B cell repertoire.
- This suggests a potential shared autoimmune mechanism or cross-reactivity in endocrine autoimmunity.
- Further research is warranted to explore the implications for autoimmune diseases like type 1 diabetes and thyroiditis.
Related Concept Videos
Hyperthyroidism I: Introduction
30
Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
30
Hyperthyroidism II: Pathophysiology
28
Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH...
28
Graves' Disease I: Introduction
23
Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence...
23
Graves Disease II: Pathophysiology
26
Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor,...
26
Type I Diabetes I: Introduction
45
Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1...
45
Type I Diabetes II: Pathophysiology
75
Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular...
75

