| pubmed-article:21357538 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21357538 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:21357538 | lifeskim:mentions | umls-concept:C0085243 | lld:lifeskim |
| pubmed-article:21357538 | lifeskim:mentions | umls-concept:C0011854 | lld:lifeskim |
| pubmed-article:21357538 | lifeskim:mentions | umls-concept:C0386482 | lld:lifeskim |
| pubmed-article:21357538 | lifeskim:mentions | umls-concept:C0039593 | lld:lifeskim |
| pubmed-article:21357538 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:21357538 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:21357538 | pubmed:dateCreated | 2011-3-22 | lld:pubmed |
| pubmed-article:21357538 | pubmed:abstractText | Although P2rx7 has been proposed as a type 1 diabetes (T1D) susceptibility gene in NOD mice, its potential pathogenic role has not been directly determined. To test this possibility, we generated a new NOD stock deficient in P2X(7) receptors. T1D development was not altered by P2X(7) ablation. Previous studies found CD38 knockout (KO) NOD mice developed accelerated T1D partly because of a loss of CD4(+) invariant NKT (iNKT) cells and Foxp3(+) regulatory T cells (Tregs). These immunoregulatory T cell populations are highly sensitive to NAD-induced cell death activated by ADP ribosyltransferase-2 (ART2)-mediated ADP ribosylation of P2X(7) receptors. Therefore, we asked whether T1D acceleration was suppressed in a double-KO NOD stock lacking both P2X(7) and CD38 by rescuing CD4(+) iNKT cells and Tregs from NAD-induced cell death. We demonstrated that P2X(7) was required for T1D acceleration induced by CD38 deficiency. The CD38 KO-induced defects in homeostasis of CD4(+) iNKT cells and Tregs were corrected by coablation of P2X(7). T1D acceleration in CD38-deficient NOD mice also requires ART2 expression. If increased ADP ribosylation of P2X(7) in CD38-deficient NOD mice underlies disease acceleration, then a comparable T1D incidence should be induced by coablation of both CD38 and ART2, or CD38 and P2X(7). However, a previously established NOD stock deficient in both CD38 and ART2 expression is T1D resistant. This study demonstrated the presence of a T1D resistance gene closely linked to the ablated Cd38 allele in the previously reported NOD stock also lacking ART2, but not in the newly generated CD38/P2X(7) double-KO line. | lld:pubmed |
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| pubmed-article:21357538 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:21357538 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21357538 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21357538 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21357538 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21357538 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21357538 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21357538 | pubmed:language | eng | lld:pubmed |
| pubmed-article:21357538 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21357538 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:21357538 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:21357538 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21357538 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21357538 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:21357538 | pubmed:issn | 1550-6606 | lld:pubmed |
| pubmed-article:21357538 | pubmed:author | pubmed-author:ReifsnyderPet... | lld:pubmed |
| pubmed-article:21357538 | pubmed:author | pubmed-author:LeiterEdward... | lld:pubmed |
| pubmed-article:21357538 | pubmed:author | pubmed-author:SerrezeDavid... | lld:pubmed |
| pubmed-article:21357538 | pubmed:author | pubmed-author:ChenYi-GuangY... | lld:pubmed |
| pubmed-article:21357538 | pubmed:author | pubmed-author:ScheupleinFel... | lld:pubmed |
| pubmed-article:21357538 | pubmed:author | pubmed-author:DriverJohn... | lld:pubmed |
| pubmed-article:21357538 | pubmed:author | pubmed-author:HewesAmanda... | lld:pubmed |
| pubmed-article:21357538 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:21357538 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:21357538 | pubmed:volume | 186 | lld:pubmed |
| pubmed-article:21357538 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21357538 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21357538 | pubmed:pagination | 4278-84 | lld:pubmed |
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| pubmed-article:21357538 | pubmed:meshHeading | pubmed-meshheading:21357538... | lld:pubmed |
| pubmed-article:21357538 | pubmed:year | 2011 | lld:pubmed |
| pubmed-article:21357538 | pubmed:articleTitle | Testing the role of P2X7 receptors in the development of type 1 diabetes in nonobese diabetic mice. | lld:pubmed |
| pubmed-article:21357538 | pubmed:affiliation | The Jackson Laboratory, Bar Harbor, ME 04609, USA. | lld:pubmed |
| pubmed-article:21357538 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:21357538 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:21357538 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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