作者: Olivier Boulard , Guy Fluteau , Laure Eloy , Diane Damotte , Pierre Bedossa
DOI: 10.4049/JIMMUNOL.168.8.4192
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摘要: The nonobese diabetic (NOD) mouse strain provides a good study model for Sjogren’s syndrome (SS). genetic control of SS was investigated in this using different matings, including (NOD × C57BL/6 (B6))F 2 cross, NZW)F and ((NOD B6) NOD) backcross. Multiple loci were detected depending on parent combination sex. Despite significant complexity, two main features prominent. First, the middle region chromosome 1 (chr.1) all crosses. Its effect most visible B6)F cross dominated over that other loci, those mapping chr.8, 9, 10, 16; these minor observed only absence NOD haplotype chr.1. Most critically, chr.1 sufficient to trigger an SS-like inflammatory infiltrate salivary glands as shown by new congenic carrying restricted segment derived from Second, several chromosomal regions previously associated with autoimmune phenotypes, Iddm (chr.1, 2, 3, 17, corresponding Idd5 , Idd13 Idd3 Idd2 Idd1 respectively), accounting strong linkage reported between insulitis sialitis, autoantibody production (chr.10 16, Bana2 Bah2 respectively). Interestingly, females chr.7 males, probably because latent predisposition NZW strain. Altogether findings reflect complexity heterogeneity human SS.