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- W11654807 abstract "Islet cells, including insulin-producing β cells, express all the TLRs and their triggering markedly increases the secretion of proinflammatory chemokines. Thus, initial events in T1D development leading to leukocyte infiltration into the pancreatic islets may be provoked by triggering of TLRs expressed by islet cells, which can respond to microbial signals by up-regulating the secretion of chemokines able to attract Th1 cells, macrophages, and DCs. Since these cell types are involved in the pathogenesis of T1D, the TLR-mediated up-regulation of proinflammatory chemokine production by islet cells appears to be an important element in the early steps of T1D development. TLR3 and TLR9 appear to be particularly active in leading to production of proinflammatory chemokines by islet cells that can contribute to create the conditions for an autoimmune attack. Our work has also shown that vitamin D analogs can significantly down-regulate in vitro and in vivo proinflammatory chemokine production by islet cells, inhibiting T cell recruitment into the pancreatic islets and T1D development. The inhibition of islet chemokine production in vivo persists after restimulation with TLR ligands and is associated with upregulation of IκBα transcription, an inhibitor of NF-κB, and with arrest of NF-κBp65 nuclear translocation, highlighting a novel mechanism of action exerted by VDR ligands potentially relevant for the treatment of T1D and other autoimmune diseases." @default.
- W11654807 created "2016-06-24" @default.
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- W11654807 date "2006-01-01" @default.
- W11654807 modified "2023-09-23" @default.
- W11654807 title "Leukocyte migration to pancreatic islets: a critical step in the pathogenesis of type 1 diabetes" @default.
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- W11654807 doi "https://doi.org/10.1007/3-7643-7442-x_10" @default.
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