Inhibiting Notch-1 reduces the expression of Toll-like receptor 9 in BABL/C-lpr mouse kidneys and improves glucocorticoid sensitivity.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease, characterized by the development of a pathogenic autoantibodies. Lupus nephritis is a major cause of mortality in patients with SLE. Glucocorticoids are used for the treatment of lupus, however, corticosteroids have no effect on the expression of Toll-like receptor 9 (TLR9), which may limit response to corticosteroids in certain patients with SLR. The expression of TLR9 can be used as a predictor of glucocorticoid response in patients with active SLE. The present study analyzed urine proteins and pathological kidney sections of BABL/C-lpr mice and found that, following the inhibition of Notch1, glucocorticoid treatment improved the symptoms of lupus nephritis. Furthermore, glucocorticoid treatment reduced the expression of TLR9 in the BABL/C-lpr mouse kidneys, according to immunohistochemical and western blot analyses. These results suggested that inhibition of the expression of Notch-1 enhanced corticosteroid sensitivity in BABL/C-lpr mice.