Objectives: Low back pain becomes a common orthopaedic disease today. It is mainly induced by the degeneration of the intervertebral disc. In this study, we tried to reveal the pathogenesis of the degeneration and the relative therapeutic strategy, which are still elusive. Materials and Methods: We collected 15 degenerative intervertebral tissues and five healthy donors. Nucleus pulposus and annulus fibrosus cells were subcultured. miR‐640 expression was determined by qPCR. Computer analysis and luciferase reporter assay were used to confirm miR‐640 target genes. Immunohistochemical and immunocytochemical staining was used to trace the proinflammatory cytokines and key transductor of signalling pathways. We also used β‐galactosidase staining, flow cytometry, and cell viability assay to monitor the degenerative index. Results: miR‐640 overexpressed in patients derived degenerative nucleus pulposus tissues and cells. The inflammatory environment promoted miR‐640 expression via NF‐κB signalling pathway. In addition, miR‐640 targeted to LRP1 and enhances NF‐κB signal activity, which built a positive feedback loop. miR‐640 inhibited the expression of β‐catenin and EP300, therefore, restrained WNT signal and induced the degeneration in nucleus pulposus cells. miR‐640 inhibitor treatment exhibited the effects of anti‐inflammation, reverse WNT signalling pathway exhaustion, and remission of degenerative characteristics in vitro. Conclusions: miR‐640 plays an important role in the degeneration of intervertebral disc and the relative inflammatory microenvironment. It is a promising potential therapeutic target for the low back pain biotherapy.

B cell activating factor (BAFF) is a cytokine of tumor necrosis factor family mainly produced by monocytes and dendritic cells. BAFF can regulate the proliferation, differentiation, and survival of B lymphocytes by binding with BAFF-R on B cell membrane. Accumulating evidences showed that BAFF played crucial roles and was overexpressed in various autoimmune diseases such as systemic lupus erythematous (SLE) and rheumatoid arthritis (RA). This suggests that BAFF may be a therapeutic target for these diseases. In the present study, we developed a BAFF therapeutic vaccine by coupling a T helper cell epitope AKFVAAWTLKAA (PADRE) to the N terminus of BAFF extracellular domains (PADRE-BAFF) and expressed this fusion protein in Escherichia coli. The purified vaccine can induce high titer of neutralizing BAFF antibodies and ameliorate the syndrome of complete Freunds adjuvant (CFA) induced rheumatoid arthritis in rats. Our data indicated that the BAFF autovaccine may be a useful candidate for the treatment of some autoimmune diseases associated with high level of BAFF.