Why Would a T Cell Destroy a β Cell? An Immunometabolic Model Based on Chronic Parasitic Infection

The classical autoimmune model of diabetes contains a fundamental conceptual gap: it does not adequately explain the initial trigger that leads highly regulated T lymphocytes to selectively attack healthy β cells. This work proposes an alternative model grounded in immunological and parasitological literature: chronic parasitic infections—common in tropical regions such as the Brazilian Amazon—can initiate persistent inflammation, molecular mimicry, tissue remodeling, and neoantigen formation, ultimately driving the loss of immune tolerance and selective destruction of β cells. This perspective introduces the concept of Parasitic-Origin Immunometabolic Diabetes (POID), integrating immunology, parasitology, and metabolism into a unified framework.