| id |
pubmed-2192620
|
| recordtype |
oai_dc
|
| spelling |
pubmed-21926202008-04-16 IL-10 is necessary and sufficient for autoimmune diabetes in conjunction with NOD MHC homozygosity Articles Contrary to expectations based on in vitro experiments, we previously found that pancreatic IL-10 did not inhibit autoimmune diabetes but accelerated it in an MHC-dependent manner. Therefore, the ability of IL- 10 to overcome the absence of all non-MHC diabetes susceptibility (Idd) alleles was studied in transgenic mice expressing pancreatic IL-10 backcrossed to B10.H2g7 congenic mice, which have no Idd alleles other than NOD MHC (H2g7). IL-10 transgenic backcross 1 (BC1) mice with H2g7/g7 haplotype developed clear-cut insulitis and diabetes, but neither transgenic mice with the H2g/b haplotype nor nontransgenic BC1 mice did so. Further implicating IL-10 in autoimmune diabetes, anti-IL- 10 antibody treatment inhibited the development of insulitis in NOD mice. These results suggest that IL-10 may be necessary and sufficient for producing autoimmune diabetes in conjunction with NOD MHC homozygosity and that some Idd genes may be related to the regulation of IL-10. The Rockefeller University Press 1996-06-01 /pmc/articles/PMC2192620/ /pubmed/8676087 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
|
| repository_type |
Open Access Journal
|
| institution_category |
Foreign Institution
|
| institution |
US National Center for Biotechnology Information
|
| building |
NCBI PubMed
|
| collection |
Online Access
|
| language |
English
|
| format |
Online
|
| title |
IL-10 is necessary and sufficient for autoimmune diabetes in conjunction with NOD MHC homozygosity
|
| spellingShingle |
IL-10 is necessary and sufficient for autoimmune diabetes in conjunction with NOD MHC homozygosity
|
| title_short |
IL-10 is necessary and sufficient for autoimmune diabetes in conjunction with NOD MHC homozygosity
|
| title_full |
IL-10 is necessary and sufficient for autoimmune diabetes in conjunction with NOD MHC homozygosity
|
| title_fullStr |
IL-10 is necessary and sufficient for autoimmune diabetes in conjunction with NOD MHC homozygosity
|
| title_full_unstemmed |
IL-10 is necessary and sufficient for autoimmune diabetes in conjunction with NOD MHC homozygosity
|
| title_sort |
il-10 is necessary and sufficient for autoimmune diabetes in conjunction with nod mhc homozygosity
|
| description |
Contrary to expectations based on in vitro experiments, we previously found that pancreatic IL-10 did not inhibit autoimmune diabetes but accelerated it in an MHC-dependent manner. Therefore, the ability of IL- 10 to overcome the absence of all non-MHC diabetes susceptibility (Idd) alleles was studied in transgenic mice expressing pancreatic IL-10 backcrossed to B10.H2g7 congenic mice, which have no Idd alleles other than NOD MHC (H2g7). IL-10 transgenic backcross 1 (BC1) mice with H2g7/g7 haplotype developed clear-cut insulitis and diabetes, but neither transgenic mice with the H2g/b haplotype nor nontransgenic BC1 mice did so. Further implicating IL-10 in autoimmune diabetes, anti-IL- 10 antibody treatment inhibited the development of insulitis in NOD mice. These results suggest that IL-10 may be necessary and sufficient for producing autoimmune diabetes in conjunction with NOD MHC homozygosity and that some Idd genes may be related to the regulation of IL-10.
|
| publisher |
The Rockefeller University Press
|
| publishDate |
1996
|
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2192620/
|
| _version_ |
1611430602316185600
|