[1]Wyatt RJ,Julian BA.IgA nephropathy[J].N Engl J Med,2013,368(25):2402-2414. [2]Szabo SJ,Kim ST,Costa GL,et al.A novel transcription factor,T-bet,directs Th1 lineage commitment[J].Cell,2000,100(6):655-669. [3]Zheng W,Flavell RA.The transcription factor GATA-3 is necessary and sufficient for Th2 cytokine gene expression in CD4 T cells[J].Cell,1997,89(4):587-596. [4]Ivanov II,McKenzie BS,Zhou L,et al.The orphan nuclear receptor RORgammat directs the differentiation program of proinflammatory IL-17+T helper cells[J].Cell,200,126(6):1121-1133. [5]Inoshita H,Kim BG,Yamashita M,et al.Disruption of smad4 expression in T cells leads to IgA nephropathy-like manifestations[J].PLoS One,2013,8 (11):e78736. [6]Lai KN.Pathogenesis of IgA nephropathy[J].Nat Rev Nephrol,2012,8(5):275-283. [7]Suzuki H,Moldoveanu Z,Hall S,et al.IgA1-secreting cell lines from patients with IgA nephropathy produce aberrantly glycosylated IgA1[J].J Clin Invest,2008,118(2):629-639. [8]沈浩,胡玲.Th1/Th2细胞平衡偏移与自身免疫性甲状腺疾病的相关性研究[J].中国实用内科杂志,2009,29(3):252-253. [9]Suzuki H,Suzuki Y,Aizawa M,et al.Th1 polarization in murine IgA nephrophthy directed by bone marrow-derived cell[J].Kidney Int,2007,72(3):319-327. [10]Holdsworth SR,Kitch AR,Tipping PG.Th1 and Th2 T helper cell subsets affect patterns of injury and outcomes in glomerulonephritis [J].Kidney Int,1999,55(4):1198-1216. [11]Matsumoto K,Kanmatsuse K.Increased urinary excretion of interleukin-17 in nephrotic patients.Nephron,2002(2),91:243-249. [12]Lin FJ,Jiang GR,Shan JP,et al.Imbalance of regulatory T cells to Th17 cells in IgA nephropathy[J].Scand J Clin Lab Invest,2012,72(3):221-229. [13]Harrington LE,Hatton RD,Mangan PR,et al.Interleukin-17 producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages [J].Nat Immunol,2005,6(11):1123-1132. |