Pediatr. praxi. 2024;25(2):75-78 | DOI: 10.36290/ped.2024.015
Type 1 diabetes is an autoimmune disease leading to the gradual destruction of beta cells and subsequent development of diabetes. Immunotherapy aims to stop the process of destruction and prevent or modify the rate of diabetes. Clinical trials have tested the effect of various agents to stop the autoimmune process. Treatment can be divided into antigenic, biological and supportive. In antigenic treatment, for example, the GAD-Alum, presenting the GAD autoantigen, or orally administered insulin are being tested. Biologic therapy includes agents that affect regulatory T lymphocytes, reduce autoimmune inflammation, and reduce the number and phenotype of autoaggressive cells. The most promising of these is teplizumab, which results in a change in the ratio of CD4+ to CD8+ T cells and a switch from autoaggressive to regulatory T cells. Other agents with potential effect include abatacept, alefacept, golimumab, rituximab or low-dose antithymocyte globulin. Verapamil has the potential to be a supportive drug to protect beta cells. Thanks to the results of immunomodulatory studies, a promising treatment for people at risk of developing type 1 diabetes is emerging that may significantly delay and perhaps even completely stop the autoimmune process. Together with population screening for preclinical stages of diabetes, it has the potential to fundamentally change pediatric diabetes care.
Accepted: April 3, 2024; Published: April 8, 2024 Show citation
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...
Go to original source...
Go to original source...
Go to PubMed...
Go to original source...
Go to PubMed...