On the other hand, enhancing CD137 signalling via stimulation of CD137 by agonistic anti-CD137 antibodies enhances the Th1 polarization of T cells, and augments the production of IFN-γ by activation of CD8+ T cells, leading to apoptosis of autoreactive B cells and DNTC which are potent drivers of proinflammatory responses in SLE. This evidence concerns the gene TNFRSF9 and systemic lupus erythematosus.