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静脉注射免疫球蛋白对1型人类免疫缺陷病毒感染中肿瘤坏死因子-α活性异常升高的体内作用。

Effects of intravenous immunoglobulin in vivo on abnormally increased tumor necrosis factor-alpha activity in human immunodeficiency virus type 1 infection.

作者信息

Aukrust P, Hestdal K, Lien E, Bjerkeli V, Nordøy I, Espevik T, Müller F, Frøland S S

机构信息

Medical Department A and Research Institute for Internal Medicine, University of Oslo, National Hospital, Rikshospitalet, Norway.

出版信息

J Infect Dis. 1997 Oct;176(4):913-23. doi: 10.1086/516510.

Abstract

The effect of a single bolus injection (0.4 g/kg) of intravenous immunoglobulin (IVIG) on the tumor necrosis factor (TNF) system in human immunodeficiency virus type 1 (HIV-1)-infected patients was investigated. At 140 h after infusion, there was a significant decrease in levels of TNF-alpha and a significant increase in levels of soluble TNF receptors (sTNFR) in both plasma and lipopolysaccharide-stimulated peripheral blood mononuclear cells (PBMC). A rapid (within 1 h) decline in expression of membrane-bound TNF-alpha and p55-TNFR on PBMC persisted throughout the study. In contrast, there was an increased expression of membrane-bound p75-TNFR after 140 h. IVIG administration also resulted in significantly increased numbers of circulating CD4 lymphocytes, correlated with down-regulation of TNF-alpha activity in PBMC supernatants. Thus, down-regulation of the abnormally increased TNF-alpha activity may be achieved by IVIG administration. Studies evaluating the possible therapeutic role of long-term TNF-alpha suppression by IVIG may be warranted in HIV-1-infected patients.

摘要

研究了静脉注射免疫球蛋白(IVIG)单次大剂量注射(0.4 g/kg)对1型人类免疫缺陷病毒(HIV-1)感染患者肿瘤坏死因子(TNF)系统的影响。输注后140小时,血浆和脂多糖刺激的外周血单核细胞(PBMC)中TNF-α水平显著降低,可溶性TNF受体(sTNFR)水平显著升高。在整个研究过程中,PBMC上膜结合TNF-α和p55-TNFR的表达迅速(1小时内)下降。相比之下,140小时后膜结合p75-TNFR的表达增加。IVIG给药还导致循环CD4淋巴细胞数量显著增加,这与PBMC上清液中TNF-α活性的下调相关。因此,通过IVIG给药可能实现异常升高的TNF-α活性的下调。评估IVIG长期抑制TNF-α的可能治疗作用的研究在HIV-1感染患者中可能是必要的。

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