Pancreatic α cells function as MHC class II-dependent antigen-presenting cells in type 1 diabetes.

Pancreatic α cells in type 1 diabetes acquire MHC class II–dependent antigen-presenting capacity, with progressive MHC-II gene up-regulation during disease progression in NOD mice and human islets.

• Why it matters: Antigen presentation is essential for T cell–mediated β cell destruction, but whether endocrine cells in inflamed islets contribute remained unclear.
• What they did: Single-cell RNA sequencing reanalysis in NOD mice and human T1D islets showed progressive MHC-II–associated gene up-regulation in α cells, supported by immunostaining and cytokine-driven JAK-STAT–dependent MHC-II induction.
• The result: Activated α cells internalized, processed, and presented exogenous antigens, gained costimulatory molecule expression, and promoted antigen-specific CD4+ T cell activation, identifying them as nonprofessional antigen-presenting cells in autoimmune diabetes.

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