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急性肾小球肾炎不同病中TNF和sTNFR的变化 被引量:1

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出处 《上海免疫学杂志》 CSCD 北大核心 2000年第5期314-314,共1页 Shanghai Journal of Immunology
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  • 1[1]Baud L, Ardaillou R. Tumor necrosis factor in renal injury. Miner Electrolyte Metab, 1995; 21: 336
  • 2[2]Gomez-Guerero C, Lopez-Armada MJ, Conzalez E, et al. Soluble IgA and IgG aggregates are catabolized by cultured rat mesangial cells and induce production of TNF-alpha and IL-6, and proliferation. J Immunol, 1994; 153: 5247
  • 3[3]Ortiz A, Bustos C, Alonso J, et al. Involvement of tumor necrosis factoralpha in the pathogenesis of experimental and human glomerulonephritis. Adv Nephrol Necker Hosp, 1995; 24: 53
  • 4[4]Karkar AM, Tam FW, Steninkasserer A, et al. Modulation of antibodymediated glomeular injury in vivo by IL-1ra, soluble IL-1 receptor, and soluble TNF receptor. Kid Int, 1995; 48: 1738
  • 5[5]Rostoke G, Ryme JC, Bagnard G, et al. Imbalances in serum proinflammatory cytokines and their soluble receptors: A putative role in the progression of idiopathic IgA nephropathy (IgAN) and Henoch-Schonlin purpura nephritis, and a potential target of immunoglobulin therapy. Clin Exp Immunol, 1998; 114: 468

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  • 1Karkar AM, Tam FW, Steninkasserer A, et al. Modulation of antibodymediated giomeular injure in vivo b IL-1 rasoluble IL-1 receptor and soluble TNF RECEPTOR [J]. Kid lnt, 1995,48 ; 1738.

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