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Objective / Hypothesis: Type 1 Diabetes involves autoimmune destruction of pancreatic β-cells, likely driven by genetic predisposition and environmental factors such as enteroviral infections. Autophagy, a cellular stress response pathway, is impaired in T1D and may influence immune recognition of β-cells. We hypothesized that modifications in β-cell autophagy, with or without viral infection, may alter human islet HLA-I expression and potentially specific HLA-I isotypes, with broader implications for altered β-cell immunogenicity.
Approach: Human pancreatic islets were infected with Coxsackievirus B3, a common enterovirus, and treated with either Bafilomycin A1 or C381 (autophagy inhibitor or enhancer, respectively). We assessed the impacts of aberrant autophagy on the surface expression of total and specific HLA-I isotypes to evaluate the impact of autophagy modulation on antigen presentation in β-cells.
Summary / Conclusions: We demonstrated that autophagy inhibition led to increased HLA-I expression in human islets, whereas autophagy stimulation reduced expression. In addition, we found that there are altered expression patterns of specific HLA-I isotypes under conditions of impaired autophagy, suggesting that autophagy plays a regulatory role in shaping β-cell antigenic presentation, with implications for T1D development and progression.
