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麻风反应状态期间血清肿瘤坏死因子-α和白细胞介素-1β水平。

Serum levels of tumour necrosis factor-alpha and interleukin-1 beta during leprosy reactional states.

作者信息

Sarno E N, Grau G E, Vieira L M, Nery J A

机构信息

Leprosy Unit, Fundaçâo Oswaldo Cruz, Rio de Janeiro, Brazil.

出版信息

Clin Exp Immunol. 1991 Apr;84(1):103-8.

PMID:2015700
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1535359/
Abstract

The possible role of cytokines in leprosy reactions was investigated by analysing the levels of tumour necrosis factor (TNF) and interleukin-1 (IL-1) in serum samples from 39 leprosy patients, 22 of them presenting either type I (upgrading) or type II (ENL) reactions. Fifty per cent of the patients showed elevated concentrations of TNF and IL-1 in at least one of the serum samples tested. This included all four patients undergoing type I reversal reaction and nine (50%) of the ENL patients studied. Concentrations of TNF above 1000 pg/ml were found in four patients with ENL. Development of erythema multiforme in these ENL patients represented an aggravating factor and all four patients suffering from this type of lesion demonstrated increased serum TNF levels. All BT patients tested presented elevated IL-1 levels, while only half of them presented elevated levels of TNF. No correlation was found between any particular systemic symptoms and the levels of TNF and IL-1. These results suggest that TNF and IL-1 may be implicated in leprosy reactions, either acting directly or in synergism with other cytokines.

摘要

通过分析39例麻风患者血清样本中肿瘤坏死因子(TNF)和白细胞介素-1(IL-1)的水平,研究了细胞因子在麻风反应中的可能作用。其中22例患者出现I型(升级型)或II型(ENL)反应。50%的患者在至少一份检测的血清样本中显示TNF和IL-1浓度升高。这包括所有4例经历I型逆转反应的患者以及9例(50%)所研究的ENL患者。在4例ENL患者中发现TNF浓度高于1000 pg/ml。这些ENL患者中多形红斑的出现是一个加重因素,所有4例患有这种类型病变的患者血清TNF水平均升高。所有检测的BT患者IL-1水平均升高,而其中只有一半患者TNF水平升高。未发现任何特定全身症状与TNF和IL-1水平之间存在相关性。这些结果表明,TNF和IL-1可能参与麻风反应,要么直接起作用,要么与其他细胞因子协同作用。

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本文引用的文献

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Inhibitory effect of corticosteroids on the secretion of tumour necrosis factor (TNF) by monocytes is dependent on the stimulus inducing TNF synthesis.皮质类固醇对单核细胞分泌肿瘤坏死因子(TNF)的抑制作用取决于诱导TNF合成的刺激因素。
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