Fig. 3

Pharmacodynamics of bortezomib in anti-NMDA receptor encephalitis. Bortezomib primarily inhibits the ubiquitin–proteasome system and the NF-kB pathway, promoting apoptosis in plasma cells and activated T cells. By blocking the 26S proteasome activity, it prevents protein degradation, leading to apoptosis and affecting NF-kB. This influences the immune response by reducing autoreactive B cells and suppressing T-cell activation and proliferation, decreasing pro-inflammatory cytokines such as IL-6 and TNF-α while increasing anti-inflammatory cytokines such as IL-10. In addition, Bortezomib enhances regulatory T-cell activity, preserving immunological tolerance and suppressing autoimmune responses