Blockade of the programmed death-1 (PD1) pathway undermines potent genetic protection from type 1 diabetes.

<h4>Aims/hypothesis</h4>Inhibition of PD1-PDL1 signaling in NOD mice accelerates onset of type 1 diabetes implicating this pathway in suppressing the emergence of pancreatic beta cell reactive T-cells. However, the molecular mechanism by which PD1 signaling protects from type 1 diabetes...

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Main Authors: Nora M Kochupurakkal, Annie J Kruger, Sudipta Tripathi, Bing Zhu, La Tonya Adams, Daniel B Rainbow, Aldo Rossini, Dale L Greiner, Mohamed H Sayegh, Linda S Wicker, Indira Guleria
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-01-01
Series:PLoS ONE
Online Access:https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0089561&type=printable
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author Nora M Kochupurakkal
Annie J Kruger
Sudipta Tripathi
Bing Zhu
La Tonya Adams
Daniel B Rainbow
Aldo Rossini
Dale L Greiner
Mohamed H Sayegh
Linda S Wicker
Indira Guleria
author_facet Nora M Kochupurakkal
Annie J Kruger
Sudipta Tripathi
Bing Zhu
La Tonya Adams
Daniel B Rainbow
Aldo Rossini
Dale L Greiner
Mohamed H Sayegh
Linda S Wicker
Indira Guleria
author_sort Nora M Kochupurakkal
collection DOAJ
description <h4>Aims/hypothesis</h4>Inhibition of PD1-PDL1 signaling in NOD mice accelerates onset of type 1 diabetes implicating this pathway in suppressing the emergence of pancreatic beta cell reactive T-cells. However, the molecular mechanism by which PD1 signaling protects from type 1 diabetes is not clear. We hypothesized that differential susceptibility of Idd mouse strains to type 1 diabetes when challenged with anti PDL1 will identify genomic loci that collaborate with PD1 signaling in suppressing type 1 diabetes.<h4>Methods</h4>Anti PDL1 was administered to NOD and various Idd mouse strains at 10 weeks of age and onset of disease was monitored by measuring blood glucose levels. Additionally, histological evaluation of the pancreas was performed to determine degree of insulitis. Statistical analysis of the data was performed using Log-Rank and Student's t-test.<h4>Results</h4>Blockade of PDL1 rapidly precipitated type 1 diabetes in nearly all NOD Idd congenic strains tested, despite the fact that all are moderately (Idd5, Idd3 and Idd10/18) or highly (Idd3/10/18 and Idd9) protected from spontaneous type 1 diabetes by virtue of their protective Idd genes. Only the Idd3/5 strain, which is nearly 100% protected from spontaneous disease, remained normoglycemic following PDL1 blockade.<h4>Conclusions</h4>These results indicate that multiple Idd loci collaborate with PD1 signaling. Anti PDL1 treatment undermines a large portion of the genetic protection mediated by Idd genes in the NOD model of type 1 diabetes. Basal insulitis correlated with higher susceptibility to type 1 diabetes. These findings have important implications since the PD1 pathway is a target for immunotherapy.
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spelling doaj-art-718088f5c03e45709c481e64578798ac2025-08-20T02:22:39ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0192e8956110.1371/journal.pone.0089561Blockade of the programmed death-1 (PD1) pathway undermines potent genetic protection from type 1 diabetes.Nora M KochupurakkalAnnie J KrugerSudipta TripathiBing ZhuLa Tonya AdamsDaniel B RainbowAldo RossiniDale L GreinerMohamed H SayeghLinda S WickerIndira Guleria<h4>Aims/hypothesis</h4>Inhibition of PD1-PDL1 signaling in NOD mice accelerates onset of type 1 diabetes implicating this pathway in suppressing the emergence of pancreatic beta cell reactive T-cells. However, the molecular mechanism by which PD1 signaling protects from type 1 diabetes is not clear. We hypothesized that differential susceptibility of Idd mouse strains to type 1 diabetes when challenged with anti PDL1 will identify genomic loci that collaborate with PD1 signaling in suppressing type 1 diabetes.<h4>Methods</h4>Anti PDL1 was administered to NOD and various Idd mouse strains at 10 weeks of age and onset of disease was monitored by measuring blood glucose levels. Additionally, histological evaluation of the pancreas was performed to determine degree of insulitis. Statistical analysis of the data was performed using Log-Rank and Student's t-test.<h4>Results</h4>Blockade of PDL1 rapidly precipitated type 1 diabetes in nearly all NOD Idd congenic strains tested, despite the fact that all are moderately (Idd5, Idd3 and Idd10/18) or highly (Idd3/10/18 and Idd9) protected from spontaneous type 1 diabetes by virtue of their protective Idd genes. Only the Idd3/5 strain, which is nearly 100% protected from spontaneous disease, remained normoglycemic following PDL1 blockade.<h4>Conclusions</h4>These results indicate that multiple Idd loci collaborate with PD1 signaling. Anti PDL1 treatment undermines a large portion of the genetic protection mediated by Idd genes in the NOD model of type 1 diabetes. Basal insulitis correlated with higher susceptibility to type 1 diabetes. These findings have important implications since the PD1 pathway is a target for immunotherapy.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0089561&type=printable
spellingShingle Nora M Kochupurakkal
Annie J Kruger
Sudipta Tripathi
Bing Zhu
La Tonya Adams
Daniel B Rainbow
Aldo Rossini
Dale L Greiner
Mohamed H Sayegh
Linda S Wicker
Indira Guleria
Blockade of the programmed death-1 (PD1) pathway undermines potent genetic protection from type 1 diabetes.
PLoS ONE
title Blockade of the programmed death-1 (PD1) pathway undermines potent genetic protection from type 1 diabetes.
title_full Blockade of the programmed death-1 (PD1) pathway undermines potent genetic protection from type 1 diabetes.
title_fullStr Blockade of the programmed death-1 (PD1) pathway undermines potent genetic protection from type 1 diabetes.
title_full_unstemmed Blockade of the programmed death-1 (PD1) pathway undermines potent genetic protection from type 1 diabetes.
title_short Blockade of the programmed death-1 (PD1) pathway undermines potent genetic protection from type 1 diabetes.
title_sort blockade of the programmed death 1 pd1 pathway undermines potent genetic protection from type 1 diabetes
url https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0089561&type=printable
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