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Immunotherapy for type 1 diabetes

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Metab Target Organ Damage 2024;4:[Accepted].
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Abstract

Type 1 diabetes mellitus (T1D) is a chronic autoimmune disorder in which the immune system attacks insulin-producing beta cells in the pancreas, leading to insulin deficiency and hyperglycemia. Despite advancements in treatment, managing T1D remains challenging, with patients experiencing diabetes distress and reduced life expectancy. Immunotherapy offers promising strategies for modifying the course of T1D by targeting the immune system's attack on beta cells. Recent highlight is teplizumab, an anti-CD3 monoclonal antibody, which delays the progression of T1D in patients with recent onset by preserving endogenous insulin production. Clinical trials have shown that teplizumab can improve glycemic control and delay the onset of stage 3 T1D for up to two years in at-risk individuals.


Other immunotherapies, including targeting B cells with rituximab, have shown potential to preserve beta cell function and reduce insulin requirements in recent-onset T1D. Additionally, T cell modulation therapies such as abatacept have been shown to slow the decline in beta cell function. Cytokine-directed therapies targeting inflammation have also demonstrated potential in preserving beta cell function and improving glycemic control. Combination therapies, such as the use of anti-IL-21 antibodies with liraglutide, may offer synergistic benefits and preserve endogenous insulin secretion. While immunotherapies offer potential for short-term protection of beta cells, ongoing research is needed to refine treatment strategies and identify optimal timing and combinations of therapies. This could lead to safer and more effective management of T1D, potentially reducing reliance on insulin therapy and providing long-term benefits for patients.

Keywords

Type 1 diabetes, immunology,  immunotherapy, teplizumab, pancreatic beta cells

Cite This Article

Sann KM, Rahman M, Thu MM. Immunotherapy for type 1 diabetes. Metab Target Organ Damage 2024;4:[Accept]. http://dx.doi.org/10.20517/mtod.2024.37

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© The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
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Metabolism and Target Organ Damage
ISSN 2769-6375 (Online)

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