Susceptibility to autoimmune disorders results from the interaction of multiple 
genetic factors that regulate the threshold of autoreactivity. Genome-wide 
microsatellite screens and large-scale single nucleotide polymorphism (SNP) 
association studies have identified chromosomal loci that are associated with 
specific disorders including systemic lupus erythematosus, rheumatoid arthritis, 
juvenile arthritis, multiple sclerosis, and diabetes. Numerous candidate gene 
association studies have in turn investigated the association of specific genes 
within these chromosomal regions, with susceptibility to autoimmune diseases 
(e.g. FcgammaReceptors, TYK2 and systemic lupus). More recently, large-scale 
differential gene expression studies performed on selected tissues from patients 
with autoimmune disorders, have led to the identification of gene signatures 
associated with the activation of specific pathways in these diseases (e.g. 
interferon signature in lupus). In the future, integrated analyses of gene (and 
protein) expression together with SNP data will allow us to sketch an 
intelligible picture of the genesis of autoimmunity in humans. This review sets 
out to illustrate how the most recent advances in the field of systemic lupus 
erythematosus, rheumatoid arthritis and juvenile arthritis have led to a better 
understanding of these disorders.