No abstract

The mechanism underlying the autoimmune polyglandular syndrome type-1 (APS1) has been attributed to defective T-cell negative selection resulting from reduced expression and presentation of autoantigens in thymic medullary epithelial cells (MECs). It has also been postulated that Aire is involved in development of regulatory T cells, although supporting evidence is lacking. Here we show that expression of Aire in MECs is required for development of iNKT cells, suggesting a role for iNKT cells in APS1.

No abstract

In the version of this article initially published, the middle panel of Figure 4d incorrectly reported the percentage of demyelination in M. lepraetreated cultures. The percentage should be 67 ± 3.1 instead of 7 ± 3.1. The error has been corrected in the HTML and PDF versions of the article.

We recently mapped Idd4 to a 5.2 cM interval on chromosome 11 with two subloci, Idd4.1 and Idd4.2, in nonobese diabetic (NOD) mice. Based on the localization of platelet-activating factor acetylhydrolase Ib1 (PAF-AHIb1) and the decreased activity of PAF-AH in type 1 diabetes (T1D) patients, we hypothesized that PAF-AHIb1 in Idd4.1 is a candidate gene. The PAF-AHIb1 gene in NOD mice was cloned and sequenced, and its expression and function were studied. No polymorphisms were detected in PAF-AHIb1 cDNA between NOD and B6 mice. The expression of PAF-AH Ib1 at the mRNA and protein levels was found to be similar in different tissues between NOD and B6 mice. PAF-AH activity does not differ in the pancreatic islets or spleen between NOD and B6 mice. Our findings suggest that PAF-AH Ib1 may not be a diabetes-susceptibility gene in the Idd4.1 sublocus.