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Crohn’s associated NOD2 gene variants are not involved in determining susceptibility to multiple sclerosis

University of Cambridge Neurology unit, Addenbrooke’s Hospital, Hills Road, Cambridge, CB2 2QQ, UK

Correspondence to:
Correspondence to:
Professor Alastair Compston;
alastair.compston@medschl.cam.ac.uk

Keywords: NOD2 gene; multiple sclerosis; Crohn’s disease

The first 150 words of the full text of this article appear below.

Autoimmune diseases, such as multiple sclerosis and Crohn’s disease, are believed to result from the effects of environmental agents acting on genetically susceptible individuals. Evidence from segregation analysis and systematic whole genome linkage studies indicates that the nature of this susceptibility is complex, involving several genes which each individually confer only modest excess risk. Recurrence risk analysis in the relatives of affected individuals¹ together with the comparison of whole genome linkage studies across these diseases² shows that there are likely to be both genes conferring an autoimmune diathesis in general and others determining precisely which autoimmune phenotype may result. On this basis it is reasonable to hypothesise that genes shown to be relevant in one autoimmune disease may be of importance in another and therefore offer themselves as potential candidates.

During the last few years striking progress has been made in unravelling the genetic basis of susceptibility to Crohn’s disease. . . . [Full text of this article]