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Volume 2, Issue 4 (2022) –

Cover Picture: An interesting alternative hypothesis poses that type 1 diabetes (T1D) is the result of a dysfunctional beta cell that is cleared by a correctly functioning immune system. In this perspective, T1D etiology becomes comparable to effective anti-tumor immunity and is not classified as an autoimmune disease. Arguments favoring this hypothesis point to a primary defect in insulin-producing beta cells as the initial trigger. This is supported by recent observations suggesting smaller pancreatic volumes in those affected or at-risk of T1D. Furthermore, clear signs of beta cell stress can be detected in those on their way to developing T1D, exemplified by an increased proinsulin-to-insulin ratio. This increased ratio suggests abnormalities in insulin processing and vesicular trafficking.
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