Figure 2.

Model for persistent versus acute infections in pancreas for promoting type I diabetes (T1D). Virus infections induce proinflammatory signaling in resident and infiltrating antigen-presenting cells of the pancreas. Persistent infections whereby viral products including enteroviral 5′ terminally deleted double-stranded RNA are maintained in tissue microenvironments to produce low-grade inflammatory signaling. Alternatively, acute infections may result in unregulated positive feedback mechanisms which produce chronic inflammation even after the virus is cleared.