Abstract

Type 1 Diabetes (T1D) is a chronic autoimmune disease characterized by the immune-mediated destruction of insulin-producing beta cells in the pancreas. Current therapeutic strategies primarily focus on glycemic control through exogenous insulin administration. However, emerging research has explored the potential of immune checkpoint inhibitors (ICIs), initially developed for cancer immunotherapy, as a novel therapeutic approach for T1D. This abstract provides a concise overview of the current landscape of ICIs in T1D therapy, highlighting their mechanisms of action, preclinical and clinical studies, challenges, and future prospects. ICIs target key immune checkpoint molecules, including CTLA-4, PD-1, and PD-L1, aiming to modulate immune responses. In T1D, these inhibitors hold the promise of reining in autoreactive T cells, thereby preserving beta cell function and slowing disease progression. Extensive preclinical investigations in murine models have demonstrated the efficacy of ICIs in preventing the autoimmune destruction of beta cells. These studies provide crucial insights into the mechanisms underlying T-cell regulation and offer a foundation for translating findings into clinical applications. In conclusion, immune checkpoint inhibitors represent a promising frontier in T1D therapy, offering a paradigm shift towards immune modulation for disease modification. This abstract provides a snapshot of the current status of ICIs in T1D research and underscores the need for ongoing investigations, precision medicine approaches, and collaborative efforts to unlock the full potential of these innovative therapies.