Introduction. Dysfunction of the B lymphocyte is considered to be involved in the pathogenesis of lupus nephritis (LN). Intrarenal B cells have been found in several forms of inflammatory kidney disease. B-cell activating factor (BAFF) regulates B lymphocyte proliferation and survival, and contributes to human autoimmune disease. Their role in renal inflammation is not well defined. Methods. Clinical parameters and renal biopsies from 62？LN patients were prospectively analyzed. We performed standard immunohistochemistry on serial paraffin tissue sections using monoclonal antibodies to CD20 and BAFF to investigate the characteristics and significance of locally infiltrating B cells and local BAFF expression in patients with LN. Results. Intrarenal B cells and/or BAFF were mainly distributed in the renal interstitium. Compared to the LN-non-B-cell/BAFF expression group, proteinuria (g/24 hour), blood urea nitrogen, serum creatinine levels, LN renal activity, and chronicity indices, were all significantly greater in the LN-B-cell/BAFF expression groups. The expression of BAFF was strongly associated with the quantity of B-cell infiltrate in the interstitium. Conclusion. As BAFF expression was strongly associated with B-cell infiltration, we hypothesize that altered B-cell differentiation and tolerance induced by excess BAFF may be central to the pathogenesis of LN. 1. Introduction Lupus nephritis (LN) in systemic lupus erythematosus (SLE) is a major cause of morbidity and end-stage renal disease [1]. LN develops in up to 60% of SLE patients during the course of the disease [2]. Dysfunction of B cells is thought to be important in the pathogenesis of SLE. B cells are also considered to be involved in LN, particularly as a source of nephritogenic auto-antibodies [3]. Intrarenal inflammation is a common feature in LN. However, little is known about the role of B cells as part of the infiltrating cell population. This might be because B cells have classically been considered to exert long-range effects, mostly via activation in secondary lymphoid organs such as lymph nodes and the spleen, with subsequent proliferation and differentiation into antibody-producing plasma cells. Studies have described the high prevalence of intrarenal B cells in immune-mediated diseases, including renal transplant rejection and glomerulonephritis [4–6]. Local B-cell infiltrates could play a role in tissue injury such as tissue fibrosis, neolymphangiogenesis, and ectopic lymphomagenesis [7]. Recently, a contribution of B cells to the formation of lymphoid-like structures in renal
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