Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Members of the tumor necrosis factor receptor superfamily play an important role in the initiation, expansion, and termination of an immune response. It has recently been demonstrated that one member of this family, CD30, plays a central role in maintaining peripheral tolerance by controlling the expansion of autoreactive CD8+ T-cells. In the present study, Cd30 was mapped to a 5.6-cM interval on chromosome 4 containing the type 1 diabetes susceptibility locus Idd9.2. We determined the intron/exon structure of Cd30 and sequenced the exons, as well as 1.8 kb of the 5' putative promoter region, from 6 different mouse strains. Remarkably, 63 sequence variants, both coding and noncoding, were found. A total of 27 sequence variants, 4 of which were nonsynonymous, were found between the diabetes susceptible NOD strain and the resistant B10 strain. Of these sequence variants, 19 are within the promoter region. However, no difference between NOD and the congenic strain NOD.B10 Idd9R1, which has the B10 allele of Cd30, was observed in CD30 expression at either the mRNA or protein level. Given its role in protecting against autoimmunity, one or more of the coding variants within CD30 is a good candidate for the Idd9.2 etiological variant.

Original publication

DOI

10.2337/diabetes.49.9.1612

Type

Journal article

Journal

Diabetes

Publisher

American Diabetes Association

Publication Date

01/09/2000

Volume

49

Pages

1612 - 1616