Abstract

Abstract Renal involvement remains the principal cause of morbidity and mortality in SLE. B cells play a prominent role in kidney pathology in mouse models of SLE. In addition to producing autoantibodies, B cells produce cytokines and can present antigen to autoreactive T cells. Recently, we identified a B cell population with high expression of CD19 and CD20 and low expression of CD21 that is expanded in some human SLE patients. The presence of an expanded CD19hi B cell population correlates with poor long-term outcomes of end stage renal disease. High expression of CXCR3 by CD19hi B cells, suggests that they are trafficking to sites of inflammation, such as the kidney. To test this possibility we examined concurrent patient urine and plasma samples for the presence of B cells by flow cytometry. An Interferon alpha assay was used to determine whether levels were elevated in blood and urine.We identified B cells in ~1/3 of patient samples that are likely of kidney origin. Patients fell into two non-overlapping groups based on B cell phenotype.In the first group, urine B cells exhibited a B cell phenotype, among which were CD19hi B cells, present at the frequency equal to the peripheral blood.In the second group, the B cells exhibited a plasmablast phenotype and these cells spontaneously secreted IgG. Moreover, IFNα levels in plasma correlate significantly with the frequency of CD19hi B cells.

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