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Decoding the immune dance: Unraveling the interplay between beta cells and type 1 diabetes. | LitMetric

Decoding the immune dance: Unraveling the interplay between beta cells and type 1 diabetes.

Mol Metab

Department of Endocrinology, Indiana University School of Medicine, Indianapolis, IN, 46202, United States. Electronic address:

Published: October 2024

Background: Type 1 diabetes (T1D) is an autoimmune disease characterized by the specific destruction of insulin-producing beta cells in the pancreas by the immune system, including CD4 cells which orchestrate the attack and CD8 cells which directly destroy the beta cells, resulting in the loss of glucose homeostasis.

Scope Of Review: This comprehensive document delves into the complex interplay between the immune system and beta cells, aiming to shed light on the mechanisms driving their destruction in T1D. Insights into the genetic predisposition, environmental triggers, and autoimmune responses provide a foundation for understanding the autoimmune attack on beta cells. From the role of viral infections as potential triggers to the inflammatory response of beta cells, an intricate puzzle starts to unfold. This exploration highlights the importance of beta cells in breaking immune tolerance and the factors contributing to their targeted destruction. Furthermore, it examines the potential role of autophagy and the impact of cytokine signaling on beta cell function and survival.

Major Conclusions: This review collectively represents current research findings on T1D which offers valuable perspectives on novel therapeutic approaches for preserving beta cell mass, restoring immune tolerance, and ultimately preventing or halting the progression of T1D. By unraveling the complex dynamics between the immune system and beta cells, we inch closer to a comprehensive understanding of T1D pathogenesis, paving the way for more effective treatments and ultimately a cure.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11342121PMC
http://dx.doi.org/10.1016/j.molmet.2024.101998DOI Listing

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