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人白细胞抑制因子(LIF)增强中性粒细胞1型和3型补体受体的功能。

Enhancement of the function of neutrophil type-1 and type-3 complement receptors by human leukocyte inhibitory factor (LIF).

作者信息

Borish L, Audera C, Rosenbaum R, Rocklin R E

机构信息

Allergy Division, New England Medical Center, Boston, Massachusetts 02111.

出版信息

Cell Immunol. 1988 May;113(2):320-8. doi: 10.1016/0008-8749(88)90030-5.

DOI:10.1016/0008-8749(88)90030-5
PMID:2834072
Abstract

The lymphokine leukocyte inhibitory factor (LIF) has previously been documented to enhance several neutrophil (PMN) functions, including stimulated chemotaxis and superoxide generation, phagocytosis and adherence of opsonized targets, and antibody-dependent cellular cytotoxicity. The present studies were designed to investigate the effects of LIF on PMN function mediated by the complement components C3b and C3bi. LIF induced a dose-dependent increase in superoxide production generated by opsonized zymosan (up to 97.1 +/- 31.4% at 16 U LIF/ml; P less than 0.01). While neither control nor LIF-treated PMN were capable of inducing phagocytosis of either C3b- or C3bi-opsonized sheep erythrocytes (E) directly, exposure to LIF caused a significant (P less than 0.05) increase in their adherence to E (137.4 and 59.4%, respectively). Specificity for complement receptor function was confirmed by the ability of anti-CR1 antibody to block adherence of LIF-treated PMN to EAC3b (77.0% inhibition) and anti-CR3 antibody to block adherence to EAC3bi (70.2% inhibition). Increased C3b and C3bi function may have been due, at least in part, to increased expression of their respective surface membrane receptors. Thus, using indirect immunofluorescence, LIF induced a 38.2% increase in fluorescence of the anti-CR1 antibody and a 96.1% increase in anti-CR3 binding. These studies describe an additional mechanism through which LIF may have an important pro-inflammatory role in vivo.

摘要

淋巴因子白细胞抑制因子(LIF)此前已有文献记载可增强多种中性粒细胞(PMN)功能,包括刺激趋化性和超氧化物生成、吞噬作用以及调理素化靶标的黏附,还有抗体依赖性细胞毒性。本研究旨在探讨LIF对由补体成分C3b和C3bi介导的PMN功能的影响。LIF诱导经调理的酵母聚糖产生的超氧化物产量呈剂量依赖性增加(在16 U LIF/ml时高达97.1±31.4%;P<0.01)。虽然对照和LIF处理的PMN均不能直接诱导吞噬C3b或C3bi调理的绵羊红细胞(E),但暴露于LIF会使其与E的黏附显著增加(P<0.05)(分别为137.4%和59.4%)。抗CR1抗体阻断LIF处理的PMN与EAC3b黏附的能力(77.0%抑制率)以及抗CR3抗体阻断与EAC3bi黏附的能力(70.2%抑制率)证实了补体受体功能的特异性。C3b和C3bi功能的增强可能至少部分归因于其各自表面膜受体表达的增加。因此,使用间接免疫荧光法,LIF使抗CR1抗体的荧光增加了38.2%,抗CRi3结合增加了96.1%。这些研究描述了LIF在体内可能具有重要促炎作用的另一种机制。

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Enhancement of the function of neutrophil type-1 and type-3 complement receptors by human leukocyte inhibitory factor (LIF).人白细胞抑制因子(LIF)增强中性粒细胞1型和3型补体受体的功能。
Cell Immunol. 1988 May;113(2):320-8. doi: 10.1016/0008-8749(88)90030-5.
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