Soluble TNFα Receptors Are Increased in Chronic Renal Insufficiency and Hemodialysis and Inhibit Neutrophil Priming by TNFα
作者： Richard A. Ward , Kenneth R. McLeish
DOI: 10.1111/J.1525-1594.1996.TB04521.X
关键词: Receptor 、 Endocrinology 、 Hemodialysis 、 Renal function 、 Azotemia 、 Superoxide 、 Internal medicine 、 Priming (immunology) 、 Immunology 、 Medicine 、 Respiratory burst 、 Tumor necrosis factor alpha 、 Medicine (miscellaneous) 、 Bioengineering 、 Biomaterials 、 Biomedical engineering 、 General Medicine
摘要: The oxidative burst of neutrophils from azotemic patients is refractory to priming by tumor necrosis factor-alpha (TNF alpha). Soluble TNF alpha binding protiens (sTNFR) accumulate in the plasma patients. To test hypothesis that these increased sTNFR concentrations inhibit activity, we measured nondialyzed patients, hemodialysis and normal subjects, determined fMet-Leu-Phe-stimulated superoxide production incubated with differing levels sT-NFR. These significantly as creatinine clearance decreased were greater than could be accounted for loss renal function alone. primed plasma, but this effect was reduced sTNFR. Neutrophils autologous incubation only partially corrected defect. We conclude a result cells also have an intrinsic functional
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