The Study Of The Relativity Between The Expression Of FcγRⅡB On B Cells And The Kidney Deficiency Rheumatoid Arthritis

The kidney governing bones and generating marrow is one important role in the theory of visceral manifestations. Traditional chinese medicine considers that kidney deficiency is one main pathogenesis of rheumatoid arthritis (RA). Lymphocytes that mature in the bone marrow are called B cells, which will play a key role in RA when lost immunological tolerance. Our previous study indicated that compared with the non-kidney deficiency individuals, the kidney deficiency RA patients will be more at risk of high-positive rheumatoid factor (RF) and positive antinuclear antibody. These events revealed the kidney deficiency RA may be positive correlation with the B cells lose immunological tolerance, but the role is still unclear.ObjectiveThe purpose of this study was to research the role of in RA, and its relativity between the expression of Fc γ R Ⅱ B on B cells and the kidney deficiency RA, and the potential role thereof. This study would provide clinical evidences for the further elucidate on immunological mechanism in the kidney deficiency RA.Methods43RA patients (26belong to kidney deficiency,17belong to non-kidney deficiency) and21healthy donors were enrolled this study. The sex structure, age, course of disease, total number of tender joints, total number of swollen joints, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), RF of the patients and healthy donors were analyzed. The anti-human CD19, CD27, Fc γ RⅡB monoclonal antibodies were used to delineation the naive B cells (CD19+D27), memory B cells (CD19+D27(?)), plasmablasts (CD1±CD27high) of peripheral B cells. Flow cytometry was used to detected the percentage of B cell subpopulations and their expression of FcγRⅡB.Result83.72%of the RA patients were female. The average age of the RA patients was44.88±10.36years. The mean value of the percentage of memory B cells in RA patients’ peripheral B cells was15.98±7.56%, and in healthy donors there was20.17±9.97%(P=0.016). The percentage of plasmablasts is positive correlation with CRP (P=0.000). The expression of FcγRⅡB which was irrelevant to the clinical data of RA patients, was significantly reduced on memory B cells and plasmablasts in the RA patients as compared to the healthy donors (50.78±13.80%vs.64.03±6.01%, P<0.001;48.59±11.65%vs.66.59±10.18%, P<0.001). After the RA patients were divided into kidney deficiency and non-kidney deficiency, the mean value of the percentage of memory B cells in kidney deficiency RA patients’ peripheral B cells was15.40±6.97%, lower than the healthy donors (P=0.015). the expression of FcγRⅡB was significantly reduced on memory B cells and plasmablasts in the kidney deficiency RA patients as compared to the healthy donors (49.65±15.86%vs.64.03±6.01%%,P=0.001;43.69±22.57%vs.66.59±10.18%, P<0.001). The non-kidney deficiency RA patients only showed significantly downregulation of the expression of FcγRⅡB on memory B cells as compared to the healthy donors (52.70±9.52%vs.64.03±6.01%, P=0.003). Compared to the naive B cells, the expression of FcγRⅡB was significantly reduced on the memory B cells and the plasmablasts in the RA patients; same as the kidney deficiency RA patients. In the healthy donors and the non-kidney deficiency RA patients there were no significant differences.ConclusionThe B cells lose immunological tolerance in the kidney deficiency RA may be positive correlation with the downregulation of FcγRⅡB on peripheral memory B cells and plasmablasts. The expression of FcγRⅡB is irrelevant to the disease activity and prognosis of RA. There probably are genetic abnormalities of FcγRⅡB in the kidney deficiency patients, thus increased the risk of developing RA. This study provided new clinical clue for the further research on immunological mechanism of the kidney deficiency RA.