Lupus nephritis (LN) is one of the most severe complications of SLE and is characterized by the production of nephritogenic autoantibodies and immune complex formation.5 Observations in a mouse model of LN demonstrated the involvement of interactions between OX40 and OX40L in the development of glomerulonephritis.6 It was also reported that blockade of OX40 activation in animal models of autoimmune disease resulted in down-regulation of the inflammatory process. This evidence concerns the gene TNFRSF4 and systemic lupus erythematosus.