Source: Rheum Dis Clin North Am 2002 Feb;28(1):111-26 Gaffney PM, Moser KL, Graham RR, Behrens TW. Division of Hematology, Oncology, and Transplantation, University of Minnesota Medical School, Minneapolis, Minnesota, USA. firstname.lastname@example.org
In recent years, we have witnessed an explosion in our understanding of the biology of SLE through the study of lupus-prone mice and the identification and subsequent narrowing of the genomic intervals likely responsible for SLE in human beings. The data from these efforts support the hypothesis that multiple genes contribute to disease susceptibility. Clearly, there is no single locus operating in all families multiplex for SLE, and the degree of ethnic and genetic heterogeneity seems to be quite significant.
In this respect, the genetics of SLE resemble those of many other complex genetic diseases. The list of candidate genes and pathways (see Table 1) implicated in the pathogenesis of SLE is expanding at a rapid rate. Understanding how alterations in these genes and pathways lead to the lupus phenotype is the primary objective of future genetic studies in SLE.
Publication Types:Review; Review Literature
PMID: 11840693 [PubMed – indexed for MEDLINE]