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. Author manuscript; available in PMC: 2023 Jan 27.
Published in final edited form as: Annu Rev Med. 2021 Nov 18;73:483–499. doi: 10.1146/annurev-med-042320-015952

Figure 2.

Figure 2

Potential mechanisms in enterovirus-infected cells that may contribute to triggering islet autoimmunity. β cells of T1D patients have an increased expression of CAR ❶. This, in turn, may lead to increased susceptibility to enterovirus infection. Once inside the cell, enterovirus infection can lead to ER stress ❷ or miRNA dysregulation ❸. Translation of viral proteins can lead to the production of viral antigens that resemble self antigens ❹. Virus infection can also lead to the increased production of DRiPs ❺. These viral proteins and DRiPs, once degraded, can be presented in the context of MHC-I and lead to aberrant recognition by adaptive immunity ❻. The influx of immune cells also leads to production of cytokines, which may in turn lead to bystander damage to both infected and uninfected cells ❼. Abbreviations: CAR, Coxsackie adenovirus receptor; DRiP, defective ribosome product; ER, endoplasmic reticulum; EV, enterovirus; miRNA, microRNA; MHC-I, major histocompatibility complex class I; T1D, type 1 diabetes.