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Current Diabetes Reviews

Editor-in-Chief

ISSN (Print): 1573-3998
ISSN (Online): 1875-6417

Review Article

Review on Monoclonal Antibodies (mAbs) as a Therapeutic Approach for Type 1 Diabetes

Author(s): Gaurav Agarwal* and Mayank Patel

Volume 20, Issue 7, 2024

Published on: 11 September, 2023

Article ID: e310823220578 Pages: 6

DOI: 10.2174/1573399820666230831153249

Price: $65

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Abstract

Monoclonal antibodies have been successfully utilized in a variety of animal models to treat auto-immune illnesses for a long time. Immune system responses will either be less active or more active depending on how the immune system is operating abnormally. Immune system hypoactivity reduces the body's capacity to fight off various invading pathogens, whereas immune system hyperactivity causes the body to attack and kill its own tissues and cells. For maximal patient compliance, we will concentrate on a variety of antibody therapies in this study to treat Type 1 diabetes (an autoimmune condition). T-cells are responsible for the auto-immune condition known as T1D, which causes irregularities in the function of β-cells in the pancreas. As a result, for the treatment and prevention of T1D, immunotherapies that selectively restore continuous beta cellspecific self-tolerance are needed. Utilizing monoclonal antibodies is one way to specifically target immune cell populations responsible for the auto-immune-driven disease (mAb). Numerous mAbs have demonstrated clinical safety and varied degrees of success in modulating autoimmunity, including T1D. A targeted cell population is exhausted by mAb treatments, regardless of antigenic specificity. One drawback of this treatment is the loss of obtained protective immunity. Immune effector cell function is regulated by nondepleting monoclonal antibodies (mAb). The antigenfocused new drug delivery system is made possible by the adaptability of mAbs. For the treatment of T1D and T-cell-mediated autoimmunity, different existing and potential mAb therapy methods are described in this article.

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