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Phenotypic alterations in pancreatic lymph node stromal cells from human donors with type 1 diabetes and NOD mice – published online 05/09/2019

Image from Postigo-Fernandez paper

Jorge Postigo-Fernandez, Donna L. Farber, Rémi J. Creusot

Type 1 diabetes, like many other autoimmune disorders, results, in part, from a failure to maintain peripheral tolerance. This failure is often associated with defects in professional antigen-presenting cells (APCs) (i.e. dendritic cells), which lose their tolerogenic potential, driving inflammatory responses. However, other, less well-known APCs (lymph node stromal cells) are particularly interesting because of their inherent capacity to induce self-tolerance. In this issue, Postigo-Fernandez et al (https://doi.org/10.1007/s00125-019-04984-w) study these cell populations in the context of autoimmune diabetes. Data collected from multiple human pancreatic lymph nodes reveal alterations in the relative frequency of these stromal cells, as well as an increase in their expression of MHC-II and programmed death-ligand 1 (PD-L1). These changes correlate with increased expression of a number of tolerance-related genes in human type 1 diabetes donors. The authors conclude that these unexpected findings could pave the way to immunotherapies targeting these cells to help re-establish peripheral tolerance.

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