| First Author | Aizawa M | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 4 | Pages | e95365 |
| PubMed ID | 24743510 | Mgi Jnum | J:215192 |
| Mgi Id | MGI:5604841 | Doi | 10.1371/journal.pone.0095365 |
| Citation | Aizawa M, et al. (2014) Uncoupling of glomerular IgA deposition and disease progression in alymphoplasia mice with IgA nephropathy. PLoS One 9(4):e95365 |
| abstractText | 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. |
