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T细胞转录因子T-bet依赖于信号转导和转录激活因子4(Stat-4)抑制急性结肠炎,但不依赖于Stat-1,采用[未提及具体的某种东西]的L4体细胞抗原。 (注:原文最后“of.”后面内容缺失,翻译可能不太完整准确)

T-Bet Is Dependent on Stat-4 Inhibiting Acute Colitis but Not Stat-1 Using L4 Somatic Antigen of .

作者信息

Endharti Agustina Tri, Permana Sofy

机构信息

Department of Parasitology, Faculty of Medicine, Brawijaya University, Indonesia.

Biomedical Central Laboratory, Faculty of Medicine, Brawijaya University, Indonesia.

出版信息

ScientificWorldJournal. 2018 Jun 7;2018:8571920. doi: 10.1155/2018/8571920. eCollection 2018.

DOI:10.1155/2018/8571920
PMID:29977172
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6011060/
Abstract

Helminths may alter the immunoinflammatory reactions of colitis. Proteins derived from have prospective therapy for colitis. The goal of this study was to interpret the protective mechanisms of L4 somatic antigen (LSA) from against an inflammatory response to the pathogenesis of DNBS-induced colitis. Colitis was actuated in mice by rectal instillation of DNBS. The mice were randomly divided into five groups containing control, DNBS alone, and three groups, with different doses of LSA (50, 100, and 200 g/mL), respectively. Mice initiated colitis by rectal administration of DNBS and after that were immunized with LSA for 14 days. Mice treated with LSA inhibited wasting disease compared with DNBS only group. of producing IFN- were reduced by LSA treatment. The level of T lymphocytes CD4IFN- cells in the LPL was significantly diminished by LSA at both 100 and 200 g/mL groups (<0.05). The mRNA expression of T-bet was significantly declined in LSA immunized mice, but not ROR-T mRNA, whereas GATA-3 expression tended to increase. The activation of STAT-4 significantly reduced LSA-treated mice but not STAT-1. It can be concluded that is required for optimal production of - in colitis.

摘要

蠕虫可能会改变结肠炎的免疫炎症反应。源自[未提及具体来源]的蛋白质对结肠炎有潜在治疗作用。本研究的目的是阐释来自[未提及具体来源]的L4体抗原(LSA)对二硝基苯磺酸(DNBS)诱导的结肠炎发病机制炎症反应的保护机制。通过直肠灌注DNBS在小鼠中引发结肠炎。小鼠被随机分为五组,包括对照组、单独使用DNBS组以及分别使用不同剂量LSA(50、100和200μg/mL)的三组。通过直肠给予DNBS使小鼠引发结肠炎,之后用LSA免疫14天。与仅使用DNBS的组相比,用LSA治疗的小鼠消瘦疾病得到抑制。LSA治疗降低了产生干扰素的[未提及具体细胞类型]的数量。在100和200μg/mL组中,LSA使肠黏膜固有层中T淋巴细胞CD4干扰素细胞的水平显著降低(<0.05)。在LSA免疫的小鼠中,T-bet的mRNA表达显著下降,但ROR-T mRNA未下降,而GATA-3表达有增加趋势。LSA治疗的小鼠中STAT-4的激活显著降低,但STAT-1未降低。可以得出结论,在结肠炎中,[未提及具体物质]是干扰素最佳产生所必需的。

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