The role of B-cell scaffold protein with ankyrin repeats 1 in collagen-induced arthritis / 中华风湿病学杂志

ABSTRACT

Objective To analyze the roles of B-cell ccaffold protein with ankyrin repeats 1 (BANK1) in collagen-induced arthritis (CIA) murine model and the correlation with disease severity.Methods CIA murine model were established and evaluated.In different disease stages,the serum levels of anti-C Ⅱ auto-antibodies and BANK1 were detected by electrochemiluminescence immunoassay(ELISA).Moreover,the expression of BANK1 mRNA in peripheral blood cells were detected by real-time polymerase chain reaction (PCR) and its correlation with clinical scores was analyzed.Then the percentage of BANK1 expression in B cells in spleen and draining lymph nodes were detected by flow cytometry and the level of BANK1 protein in spleen was detected by Western blotting according to the results afore mentioned.The data was analyzed by Statistical Product and Service Solutions (SPSS) Stastistics 21.0 and figures were made with Graph Pad Prism 6.Repeated measure ANOVA was used to assess differences between the two groups.Correlations were analyzed by Spearman correlation analysis.Linear regression analysis was done when a correlation was identified.Results The incidence of CIA was over 90％.The clinical scores of arthritic mice was positively correlated with the serum levels of anti C Ⅱ total IgG antibody (r=0.717 5,P ＜0.01),anti C] IgG2a antibody (r=0.675 3,P＜0.01) and anti C Ⅱ IgG2b antibody (r=0.889 4,P＜0.01) respectively.The BANK1 level in the serum and the BANK1 mRNA expression were significantly decreased in different disease stages in CIA mice when compared with normal mice.The negative correlation between the BANK1 mRNA expression and clinical scores (r=-0.485 4,P＜0.01) was observed.The percentage of BANK1 +CD19+ cells in spleen and draining lymph nodes and the level of BANK1 protein in spleen were reduced in CIA as well.Conclusion Along with the disease progress in CIA,BNK1 expression is declined,which weakens the negative regulation of BANK1 on B cells.This change goes hand in hand with the severity of arthritis.