| ObjectiveTo explore the role of kidney deficiency in the activation of B lymphocyte in patients with rheumatoid arthritis,to provide clinical evidence for re-vealing the pathogenesis of rheumatoid arthritis,and to provide a scient-ific basis for Chinese medicine to treat rheumatoid arthritis from Kidney-treating therapy.MethodsThis study included in 57 patients with rheumatoid arthritis,according to the diagnostic criteria for TCM syndrome types are divided into the kidney decificiency and no kidney deficiency,collect sex structure,age distribution,course of the disease,the number of swollen joints,the number of tenderness joints,anti-CCP antibody and rheumatoid factor(RF),erythrocyte sedimentat-ion rate(ESR),C-reactive protein(CRP),disease activity score(DAS28),and collected blood samples from patients with 2ml,then extracted the peripheral blood mononuclear cells(PBMC)from the patient’ s blood samples,and after 48 hours of culture with stimulation of IgM,then fluorescent staining was performed,the expression of CD32B and CD86 was detected by flow cytometry.Results1.In this study,57 patients with RA were enrolled,including 13 males and 44 females,and the gender ratio was 1:3.38;27 patients with kidney deficiency and 30 cases of no kidney deficiency.The average age of the patients in the kidney deficiency group was 57.04±9.80,which was significantly higher than the no kidney deficiency group(50.87±9.87 years),P=0.022,the difference was statistically significant.But there was no statistical difference between the onset age and the course of the disease,the swelling joint count,the count of the pain joint,the CRP,ESR,DAS28ESR,DAS28CRP and the auto-antibody RF and Anti-CCP ’ in the no kidney deficiency and kidney deficiency(P>0.05).2.After the stimulation of peripheral blood B lymphocyte of RA patients with IgM,there was a negative correlation between the expression rate of FcgammaRIIB and CD86 in B cells(r=-0.528,P=0.000).3.After IgM stimulation culture,the expression rate of CD86 in naive B cells with kidney deficiency group was significantly higher than that of no kidney deficiency group(P=0.000).But in memory B cells and plasmablasts,there was no difference in the expression rate of CD86 in the two groups(P=0.891、P=0.177).4.After IgM stimulation culture,the MFI of FcgammaRIIB in naive B cells with kidney deficiency group was significantly lower than that of no kidney deficiency group(P=0.026),but in memory B cells and plasmablasts with the two groups were not different(P>0.05).5.After IgM stimulation culture,the expression rate of FcgammaRIIB in memory B cells was significantly lower naive B cells in kidney deficiency g-roup(P=0.000),however,this difference does not exist in the no kidney de-ficiency group(P=0.278).And the expression rate of FcgammaRIIB in two groups of plasmablasts was significantly lower than that of naive B cells and memory B cells(P<0.05).6.After IgM stimulation culture,in the FcgammaRIIB expression rate of memory B cells,kidney deficiency group with low titers anti-CCP was signi-ficantly higher than the patients with high titers anti-CCP patients(P=0.001),rather than the no kidney deficiency group,the FcgammaRIIB expression rate between low titers and high titers anti-CCP was no difference(P=0.82).ConclusionIn summary,our studies confirm that kidney deficiency can promote the excessive activation of B cells,leading to autoimmune reaction of hyperth-yroidism,at the same time,the expression of FcgammaRIIB negative correlation with B cell activation degree and suggest possible kidney deficiency via re-ducing the FcgammaRIIB expression to promote the excessive activation of B cells,so as to increase their own immune response.And,the decrease in the expression of FcgammaRIIB in patients with kidney deficiency rheumatoid art-hritis was closely related to the increase of auto-antibody level.This sug-gests that FcgammaRIIB may be an important target for rheumatoid arthritis from kidney treatment. |
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