Abstract
Previous clinical and experimental studies have indicated that cells responsible for IgA nephropathy (IgAN), at least in part, are localized in bone marrow (BM). Indeed, we have demonstrated that murine IgAN can be experimentally reconstituted by bone marrow transplantation (BMT) from IgAN prone mice in not only normal mice, but also in alymphoplasia mice (aly/aly) independent of IgA+ cells homing to mucosa or secondary lymphoid tissues. The objective of the present study was to further assess whether secondary lymph nodes (LN) contribute to the progression of this disease. BM cells from the several lines of IgAN prone mice were transplanted into aly/aly and wild-type mice (B6). Although the transplanted aly/aly showed the same degree of mesangial IgA and IgG deposition and the same serum elevation levels of IgA and IgA-IgG immune-complexes (IC) as B6, even in extent, the progression of glomerular injury was observed only in B6. This uncoupling in aly/aly was associated with a lack of CD4+ T cells and macrophage infiltration, although phlogogenic capacity to nephritogenic IC of renal resident cells was identical between both recipients. It is suggested that secondary LN may be required for the full progression of IgAN after nephritogenic IgA and IgA/IgG IC deposition.
Highlights
IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis and exhibits mesangial IgA and IgG codeposition [1]
These data suggest that BM cells (BMC) can directly reconstitute glomerular IgA deposition and the homing process in the lamina propria (LP) is not required as reported in our previous study [24]
Several studies have shown that the number of IgA1+ plasma cells increased in the bone marrow (BM) of patients with IgAN [4,5] and that bone marrow transplantation (BMT) or peripheral blood stem cell transplantation in patients with leukemia and IgAN resulted in a remission of the leukemia as well as the IgAN [6,7], suggesting that the producing cells of nephritogenic IgA may be in the BM of IgAN
Summary
IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis and exhibits mesangial IgA and IgG codeposition [1]. Several studies have shown the numbers of IgA1+ plasma cells are increased in the bone marrow (BM) of patients with IgAN [4,5]. Bone marrow transplantation (BMT) or peripheral blood stem cell transplantation in patients with leukemia and IgAN has resulted in a remission of leukemia as well as IgAN [6,7]. These findings suggest that the cells responsible for producing pathogenic IgA1 may exist, at least in part, in the BM of IgAN patients
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