Our initial hypothesis was that the overproduced sE-selectin would interfere with monocyte and/or lymphocyte infiltration of the affected kidneys through competitive inhibition of E-selectin binding of ligands such as E-selectin ligand-1 (ESL-1) and P-selectin glycoprotein ligand (PSGL-1), thereby inhibiting the development of lupus nephritis and vasculitis in Tg MRL/lpr mice. The gene discussed is SELE; the disease is vasculitis.