Abstract
The autoimmune reaction against the beta cells of the pancreatic islets in type 1 diabetes mellitus (T1DM) patients is active in prediabetes and during the development of the clinical manifestation of T1DM, but it decreases within a few years of the clinical manifestation of this disease. A key role in the pathogenesis of T1DM is played by regulatory T cell (Treg) deficiency or dysfunction. Immune interventions, such as potential therapeutic applications or the induction of the Treg-cell population in T1DM, will be important in the development of new types of treatment. The aim of this study was to evaluate innovative immune interventions as treatments for T1DM. After an evaluation of full-length papers from the PubMed database from 2010 to 2021, 20 trials were included for the final analysis. The analysis led to the following conclusions: Treg cells play an important role in the limitation of the development of T1DM, the activation or application of Tregs may be more effective in the early stages of T1DM development, and the therapeutic use of Treg cells in T1DM is promising but requires long-term observation in a large group of patients.
Highlights
type 1 diabetes mellitus (T1DM) is becoming widespread, with approximately 490,000 children affected worldwide [1]
T1DM is an autoimmune disease that leads to the destruction of insulin-secreting pancreatic beta cells
The therapy resulted in beta-cell regeneration, insulin production, and a strong decrease in therapeutic insulin intake
Summary
T1DM is becoming widespread, with approximately 490,000 children affected worldwide [1]. T1DM is an autoimmune disease that leads to the destruction of insulin-secreting pancreatic beta cells. Insulin is an important anabolic hormone that affects glucose, lipid, protein, and mineral metabolism, as well as growth. Via insulin receptors, allows glucose to enter muscle and adipose cells; it stimulates the liver to store glucose as glycogen and synthesize fatty acids, and it stimulates the uptake of amino acids, inhibits the breakdown of fat in adipose tissue, and stimulates the uptake of potassium into cells. The selective destruction of insulin-producing pancreatic beta cells underlies T1DM, which is a genetically determined multifactorial disease. Environmental factors, e.g., viral and bacterial infections, food components, drugs, and toxins, which merely seem to trigger the onset of the disease, play an important role in its development [1,2]
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