The cutaneous forms of lupus erythematosus (LE) are true complex traits, su
sceptibility to which is determined by multiple factors. Good evidence exis
ts for both genetic and environmental components to this complexity. Severa
l different experimental techniques have found the strongest genetic associ
ations with cutaneous LE to include sequence polymorphisms of genes encodin
g HLA, TNF-alpha and complement molecules, particularly in anti-Ro-positive
patients. Abnormal expression of multiple other cytokines, adhesion molecu
les and cellular proteins (such as Ro and La) points towards a range of can
didate genes that are currently being examined in cutaneous LE. Combination
s of specific polymorphisms of genes encoding these immunoregulatory molecu
les may determine individual susceptibility to LE.