A recent study also showed that anti-OX40 therapy controlled the extent of T-cell–mediated damage in LN.17 CD4+ T-cells expressing OX40 could mediate LN either by aiding B-cells to produce antibodies, including anti-dsDNA antibodies, that may contribute to the kidney lesions18 ; or by directly infiltrating glomerular endothelial cells after ligation with OX40L, thereby causing direct damage.19 Here, TNFRSF4 is linked to medical procedure.