[Immunogenetic bases of systemic lupus erythematosus in humans].

INTRODUCTION

Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown pathogenesis. Familial studies and concordance rates among affected twins suggest that human SLE has a strong genetic basis.

CURRENT KNOWLEDGE AND KEY POINTS

Recent studies have emphasized that SLE, like other autoimmune diseases, is a complex genetic trait with contributions of both major histocompatibility complex (MHC) associated genes and multiple non-MHC genes. Recent significant advances have been made in the genetic analysis of complex traits, which allow the identification of new candidate genes in SLE. Among the genes reviewed in this article, some polymorphisms of Fc gamma receptor genes and other genes or loci localized on the long arm of the human chromosome 1 appear to be very promising.

FUTURE PROSPECTS AND PROJECTS

The identification of new susceptibility genes in SLE will certainly provide important insights into the breakdown of self-tolerance mechanisms leading to autoimmune diseases. To achieve this objective, the recruitment of a large number of genetic traits of multiplex families presenting with SLE is therefore essential. More than 125 multiplex families have been collected to date in France.