Genetic progress towards the molecular basis of autoimmunity

被引:64
作者
Pearce, SHS
Merriman, TR
机构
[1] Univ Newcastle Upon Tyne, Inst Human Genet, Int Ctr Life, Newcastle Upon Tyne NE1 3BZ, Tyne & Wear, England
[2] Univ Otago, Dept Biochem, Dunedin 9001, New Zealand
基金
英国惠康基金;
关键词
D O I
10.1016/j.molmed.2005.12.005
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The past few years have seen the identification of PTPN22 and the confirmation of CTLA-4 as common autoimmune disease genes. Together with MHC and INS, these developments have increased the collection of confirmed susceptibility loci for autoimmunity. In this article, the latest developments related to these genes and to other recently studied candidate autoimmune susceptibility loci (PDCD1, FCRL3, SUMO4, CD25, PAD14 and SLC22A4) are reviewed. Collectively, these genes strongly indicate that aberrant inhibition of the signalling cascade initiated by activation of the T-cell receptor is involved in the aetiology of autoimmune disease. However, much basic genetic, molecular and clinical research is still needed to help us fully understand the underlying mechanisms of autoimmunity and how these translate into prognosis or therapy.
引用
收藏
页码:90 / 98
页数:9
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