Author/Authors :
Sergey Nejentsev، نويسنده , , Cristian Guja، نويسنده , , Rose McCormack، نويسنده , , Jason Cooper، نويسنده , , Joanna MM Howson، نويسنده , , Sarah Nutland، نويسنده , , Helen Rance، نويسنده , , Neil Walker، نويسنده , , Dag Undlien، نويسنده , , Kjersti S Ronningen، نويسنده , , Eva Tuomilehto-Wolf، نويسنده , , Jaakko Tuomilehto، نويسنده , , Constantin Ionescu-Tirgoviste، نويسنده , , Edwin AM Gale، نويسنده , , Polly J Bingley، نويسنده , , Kathleen M Gillespie، نويسنده , , David F. Savage، نويسنده , , Dennis A. Carson، نويسنده , , Chris C. Patterson، نويسنده , , Jaume Segura
Peter Maxwell
، نويسنده , , et al.، نويسنده ,
Abstract :
Intercellular adhesion molecule-1 (ICAM-1) functions via its ligands, the leucocyte integrins, in adhesion of immune cells to endothelial cells and in T cell activation. The third immuno-globulin-like extracellular domain binds integrin Mac-1 and contains a common non-conservative aminoacid polymorphism, G241R. Phenotypically, ICAM-1 has been associated with type 1 diabetes, a T-cell-mediated autoimmune disease. We assessed two independent datasets, and noted that R241 was associated with lower risk of type 1 diabetes than is G241 (3695 families, relative risk 0•91, p=0•03; 446 families, 0•60, p=0•006). Our data indicate an aetiological role for ICAM-1 in type 1 diabetes, which needs to be confirmed in future genetic and functional experiments.
