Previous studies indicated that bone marrow cells may contribute to the pathogenesis of IgA nephropathy (IgAN). However, the cell types and mechanisms responsible remain unclear. Our recent study showed that 'grouped ddY mice' is a useful model to approach the pathogenesis of IgAN. Moreover, we also reported that bone marrow transplantation (BMT) from the onset mice of this model reconstituted IgAN in healthy recipients with strong Th1-polarization. We aimed to examine the roles of bone marrow (BM) cells, mucosa and lymphoid tissues in IgAN. We employed onset ddY mice and mutant mice lacking all systemic lymph nodes, Payer's patch, isolated lymphoid follicles in the lamina propria (LP) and IgA producing cells. BM cells from the onset mice were transplanted into the mutant and wild type (C57BL/6:B6). After BMT, serum elevation of IgA and IgA(+)B220(-) plasma cells in BM, but not IgA producing cells in LP, were observed in the mutant mice. Although both transplanted mice showed mesangial IgA deposition, glomerular lesions with IgG2a co-deposition were detected only in B6 mice. The present results suggest that glomerular IgA deposition, but not glomerular damage, can be induced by BM-derived or -primed IgA-producing cells independently of priming in mucosa and secondary lymphoid tissues.