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B 和 T 淋巴细胞衰减因子调节抗原诱导的实验性结膜炎的发展。

B and T lymphocyte attenuator regulates the development of antigen-induced experimental conjunctivitis.

机构信息

Department of Ophthalmology and Visual Science, Kochi Medical School, Kohasu, Oko-cho, Nankoku-shi, Kochi 783-8505, Japan.

出版信息

Graefes Arch Clin Exp Ophthalmol. 2012 Feb;250(2):289-95. doi: 10.1007/s00417-011-1695-8. Epub 2011 Jul 22.

DOI:10.1007/s00417-011-1695-8
PMID:21779950
Abstract

PURPOSE

To investigate the roles that B and T lymphocyte attenuator (BTLA) and herpesvirus entry mediator (HVEM) play in the development of antigen-induced experimental conjunctivitis (EC).

METHODS

BALB/c mice were immunized with ragweed (RW) in alum. Ten days later, the mice were challenged with RW in eye drops. After 24 hours, the conjunctivas, blood and spleens were collected for histological analysis, measurement of serum immunoglobulin (Ig) levels, and both flow cytometric analysis and cytokine assays, respectively. The mice were injected intraperitoneally with anti-BTLA antibody, anti-HVEM antibody or control antibody during either induction phase or effector phase.

RESULTS

Induction-phase treatment with anti-BTLA antibody but not anti-HVEM antibody significantly increased conjunctival eosinophil infiltration. Treatment with either antibody during the effector phase did not affect conjunctival eosinophil infiltration. Anti-BTLA antibody treatment during the induction phase reduced the B cell compartment and increased the CD11b-positive cell compartment in splenocytes. Additionally, anti-BTLA treatment upregulated IL-4 and IL-10 production of splenocytes stimulated by RW.

CONCLUSIONS

BTLA regulated the development of EC possibly by downregulating Th2 cytokine production and adjusting the compartments of immunocompetent cells. The regulation of EC by BTLA may be mediated by BTLA ligands other than HVEM.

摘要

目的

研究 B 和 T 淋巴细胞衰减因子(BTLA)和疱疹病毒进入介体(HVEM)在抗原诱导的实验性结膜炎(EC)发展中的作用。

方法

BALB/c 小鼠用豚草(RW) Alum 免疫。10 天后,用 RW 滴眼剂对小鼠进行攻毒。24 小时后,收集结膜、血液和脾脏进行组织学分析、血清免疫球蛋白(Ig)水平测定,以及分别进行流式细胞术分析和细胞因子测定。在诱导期或效应期,小鼠分别腹腔内注射抗 BTLA 抗体、抗 HVEM 抗体或对照抗体。

结果

诱导期抗 BTLA 抗体治疗而非抗 HVEM 抗体治疗显著增加了结膜嗜酸性粒细胞浸润。在效应期用任何一种抗体治疗均不影响结膜嗜酸性粒细胞浸润。诱导期抗 BTLA 抗体治疗减少了脾细胞中的 B 细胞群,并增加了 CD11b 阳性细胞群。此外,抗 BTLA 治疗上调了 RW 刺激的脾细胞中 IL-4 和 IL-10 的产生。

结论

BTLA 通过下调 Th2 细胞因子的产生和调整免疫活性细胞的隔室来调节 EC 的发展。BTLA 对 EC 的调节可能是通过 HVEM 以外的 BTLA 配体介导的。

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