Autoimmune diseases of the nervous system are a category of conditions in which a malfunction of the body's immune system leads to damage of nerve tissues, with B cells playing a critical role in their pathogenesis. Currently, the therapeutic approaches used in clinical practice (such as monoclonal antibodies targeting B cells) can effectively control the progression of these diseases, but fail to achieve a radical cure. Chimeric antigen receptor (CAR)-T cell therapy uses genetic engineering to modify T cells derived from either patients or donors, enabling them to specifically target and durably eliminate peripheral B cells, which might remit or even functionally cure these diseases. Currently, multiple clinical studies on efficacy and safety of CAR-T cell therapy in neurological autoimmune diseases have been carried out successively, and initial results have been achieved. This article reviews the clinical research progress in this field, discusses its application prospects and challenges, aiming to provide some references for in-depth research in this area.

Autoimmune diseases of the nervous system are a category of conditions in which a malfunction of the body's immune system leads to damage of nerve tissues, with B cells playing a critical role in their pathogenesis. Currently, the therapeutic approaches used in clinical practice (such as monoclonal antibodies targeting B cells) can effectively control the progression of these diseases, but fail to achieve a radical cure. Chimeric antigen receptor (CAR)-T cell therapy uses genetic engineering to modify T cells derived from either patients or donors, enabling them to specifically target and durably eliminate peripheral B cells, which might remit or even functionally cure these diseases. Currently, multiple clinical studies on efficacy and safety of CAR-T cell therapy in neurological autoimmune diseases have been carried out successively, and initial results have been achieved. This article reviews the clinical research progress in this field, discusses its application prospects and challenges, aiming to provide some references for in-depth research in this area.

Objective To explore the mechanism of fire needle in treating cartilage degeneration in knee osteoarthritis(KOA)based on p38MAPK signaling pathway.Methods Totally 30 SPF grade male SD rats were randomly divided into blank group,model group and fire needle group,with 10 rats in each group.The model group and fire needle group established KOA models by injecting papain into the knee joint cavity.The fire needle group received fire needle intervention in"Neixiyan"and"Dubi",while the model group and blank group only received fixation and no intervention,once every 3 days,for 4 consecutive weeks.Morphological changes in the knee joint cartilage were observed using HE staining and safranine O-solid green staining,TUNEL staining was used to detect the apoptosis index of chondrocytes,immunohistochemical staining was used to detect the expressions of p-p38 and Fas protein,qPCR was used to detect the expressions of p38 and Fas mRNA.Results Compared with the blank group,the surface of the knee joint cartilage in the model group rats was uneven,with irregular and uneven arrangement of chondrocytes,lighter matrix red staining,and unclear tidal lines,the improved Mankin's score significantly increased(P<0.001),the apoptosis index of chondrocytes significantly increased(P<0.01),the expressions of p-p38 and Fas protein in knee joint cartilage tissue significantly increased(P<0.01),and the expressions of p38 and Fas mRNA significantly increased(P<0.001).Compared with the model group,the surface of the knee joint cartilage of the fire needle group rats was relatively flat,the arrangement of chondrocytes was generally normal,and the matrix staining was slightly lighter,the improved Mankin's score significantly decreased(P<0.001),the apoptosis index of chondrocytes significantly decreased(P<0.01),the expressions of p-p38 and Fas protein in knee joint cartilage tissue significantly decreased(P<0.01),and the expressions of p38 and Fas mRNA significantly decreased(P<0.001).Conclusion Fire needle may delay the progression of KOA by inhibiting the activation of p38MAPK signaling pathway and reducing chondrocyte apoptosis of knee joint.