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- W3175869334 abstract "Purpose of review Type 1 diabetes (T1D) results from the loss of immune tolerance to pancreatic beta-cells leading to their destruction. Immune intervention therapies tested in T1D so far delayed progression but failed to restore tolerance, which partly explains their lack of durable clinical efficacy. Recent findings The role of beta-cells and islets themselves in dialogue with their micro- and macro-environment including the immune system and the intestinal microbiome is increasingly evident. Indeed, islets can both maintain and break immune tolerance. Some recent immune therapies in cancer that block immune regulation also break tolerance. Induction of immune tolerance requires activating immune activation too, whereas immune suppression precludes this process. Immunotherapy alone my not suffice without engaging islets to restore tolerance and preserve beta-cell function. Summary New insight into the role of islet tissue and its interaction with its environment in preserving or breaking tolerance has contributed to understand the development of islet autoimmunity and T1D. Knowing which factors in islets and the immune system contribute to maintaining, breaking, and restoring the balance in the immune system is critical to prevent initiation and reverse disease progression, and guides the design of novel tolerogenic strategies for durable therapeutic intervention and remission that target both the immune system and distressed islets." @default.
- W3175869334 created "2021-07-05" @default.
- W3175869334 creator A5023576332 @default.
- W3175869334 creator A5027688954 @default.
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- W3175869334 date "2021-08-01" @default.
- W3175869334 modified "2023-10-14" @default.
- W3175869334 title "Breaking and restoring immune tolerance to pancreatic beta-cells in type 1 diabetes" @default.
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- W3175869334 doi "https://doi.org/10.1097/med.0000000000000646" @default.
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