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肥大细胞脱颗粒及T细胞RANTES在口腔扁平苔藓中的作用

Mast cell degranulation and the role of T cell RANTES in oral lichen planus.

作者信息

Zhao Z Z, Sugerman P B, Zhou X J, Walsh L J, Savage N W

机构信息

School of Dentistry, The University of Queensland, Brisbane, Australia.

出版信息

Oral Dis. 2001 Jul;7(4):246-51.

Abstract

OBJECTIVES

The present study investigated mast cell degranulation in oral lichen planus (OLP) and the effect of OLP lesional T cell supernatants on mast cell degranulation.

MATERIALS AND METHODS

Immunohistochemistry was used to identify mast cell degranulation in both OLP (n = 22) and normal control (n = 14) tissues. OLP lesional T cell lines (n = 5) and HMC-1 (a human leukemia mast cell line) were used to examine the effects of OLP T cell supernatants on mast cell degranulation in vitro.

RESULTS

Approximately 60% of mast cells were degranulated in OLP. OLP lesional T cells expressed mRNA for RANTES, and TNF-alpha stimulation upregulated OLP lesional T cell RANTES secretion. OLP lesional T cell supernatants induced degranulation of HMC-1 with release of TNF-alpha and histamine. Human recombinant RANTES similarly induced mast cell degranulation. Anti-RANTES antibody blocked OLP lesional T cell supernatant-induced mast cell degranulation.

CONCLUSIONS

This study is the first to show that OLP lesional T cells produce and secrete RANTES which triggers human mast cell degranulation. Degranulating mast cells release TNF-alpha which upregulates OLP lesional T cell RANTES secretion. Such a cyclical mechanism may underlie disease chronicity and future therapies may include blocking RANTES or TNF-alpha activity in OLP.

摘要

目的

本研究调查口腔扁平苔藓(OLP)中肥大细胞脱颗粒情况以及OLP病损T细胞上清液对肥大细胞脱颗粒的影响。

材料与方法

采用免疫组织化学方法鉴定OLP组织(n = 22)和正常对照组织(n = 14)中的肥大细胞脱颗粒情况。利用OLP病损T细胞系(n = 5)和HMC-1(一种人白血病肥大细胞系)在体外检测OLP T细胞上清液对肥大细胞脱颗粒的影响。

结果

OLP中约60%的肥大细胞发生脱颗粒。OLP病损T细胞表达RANTES的mRNA,肿瘤坏死因子-α(TNF-α)刺激可上调OLP病损T细胞RANTES的分泌。OLP病损T细胞上清液诱导HMC-1脱颗粒,并释放TNF-α和组胺。人重组RANTES同样可诱导肥大细胞脱颗粒。抗RANTES抗体可阻断OLP病损T细胞上清液诱导的肥大细胞脱颗粒。

结论

本研究首次表明,OLP病损T细胞产生并分泌RANTES,后者触发人肥大细胞脱颗粒。脱颗粒的肥大细胞释放TNF-α,进而上调OLP病损T细胞RANTES的分泌。这种循环机制可能是疾病慢性化的基础,未来的治疗可能包括阻断OLP中RANTES或TNF-α的活性。

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