Open AccessAnti-macrophage migration inhibitory factor reduces transforming growth factor- 1 expression in experimental IgA nephropathy
Author(s) -
Joseph C.K. Leung,
Loretta Y.Y. Chan,
Anita W.L. Tsang,
Enmei Liu,
Man Fai Lam,
Sydney C.W. Tang,
K.N. Lai
Publication year - 2004
Publication title -
nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfh323
Subject(s) - macrophage migration inhibitory factor , nephropathy , glomerulonephritis , immune system , medicine , immunoglobulin a , antibody , endocrinology , mesangial cell , proteinuria , mesangial proliferative glomerulonephritis , cytokine , immunology , immunoglobulin g , kidney , diabetes mellitus
In human glomerulonephritis, including immunoglobulin-A nephropathy (IgAN), glomerular expression of macrophage migration inhibitory factor (MIF) is found to correlate with progressive renal injury. We have shown previously that polymeric IgA is capable of inducing MIF production in cultured human mesangial cells, suggesting a role in inducing inflammatory injury in IgAN. Herein, we examined whether IgA deposition and the subsequent renal injury can be ameliorated with anti-MIF treatment in an experimental murine model of IgAN.
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