Investigation of mechanisms by which BTLA inhibit autoimmunity and development of potential therapeutic applications

研究 BTLA 抑制自身免疫的机制并开发潜在的治疗应用

• 批准号: 21591263
• 负责人: WATANABE Norihiko
• 金额: $ 2.91万
• 依托单位: Chiba University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2009
• 资助国家: 日本
• 起止时间: 2009 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21591263/
• 关键词: BTLA; 副刺激分子; 自己免疫疾患; 免疫寛容; 樹状細胞; MRL/lprマウス; ノックアウトマウス; 自然免疫; NKT細胞

Recently, we have identified B and T lymphocyte attenuator (BTLA) as a novel inhibitory coreceptor expressed on lymphocytes. In this study, we found that the lack of BTLA exaggerates the systemic autoimmunity in lupus-prone MRL-lpr/lpr mice. In addition, we found that BTLA is also expressed on dendritic cells and serves inhibitory functions in dendritic cells. These results demonstrate that BTLA plays a protective role in autoimmune diseases and also suggest potential therapeutic applications of BTLA.

最近，我们已经确定B和T淋巴细胞衰减剂（BTLA）作为一种新的抑制性共受体表达的淋巴细胞。在这项研究中，我们发现BTLA的缺乏夸大了狼疮易感的MRL-lpr/lpr小鼠的全身性自身免疫。此外，我们发现BTLA也在树突状细胞上表达，并在树突状细胞中起抑制作用。这些结果表明，BTLA在自身免疫性疾病中起着保护作用，也表明BTLA的潜在治疗应用。

项目成果

Lack of E and T lymphocyte attenuator exacerbates autoimmune disorders and induces Fas-independent liver injury in MRL-lpr/lpr mice.

E 和 T 淋巴细胞衰减因子的缺乏会加剧 MRL-lpr/lpr 小鼠的自身免疫性疾病并诱导 Fas 依赖性肝损伤。

• 发表时间: 2011
• 作者: Watanabe N;Oya Y;Ikeda K;Hirose K;Kishimono T;NakaiimaH.;他2名
• 通讯作者: 他2名

A functional polymorphism in B and T lymphocyte attenuator is associated with susceptibility to rheumatoid arthritis.

• DOI: 10.1155/2011/305656
• 发表时间: 2011
• 期刊: Clinical & developmental immunology
• 作者: Oki M;Watanabe N;Owada T;Oya Y;Ikeda K;Saito Y;Matsumura R;Seto Y;Iwamoto I;Nakajima H
• 通讯作者: Nakajima H

A method of identifying a compound for prevening and/or treating an autoimmune disease

鉴定用于预防和/或治疗自身免疫性疾病的化合物的方法

• 发表时间: 2010

Activation‐induced accumulation of B and T lymphocyte attenuator at the immunological synapse in CD4+ T cells

• DOI: 10.1189/jlb.0309138
• 发表时间: 2010-03
• 期刊: Journal of Leukocyte Biology
• 影响因子: 5.5
• 作者: T. Owada;N. Watanabe;Mie Oki;Yoshihiro Oya;Y. Saito;T. Saito;I. Iwamoto;T. Murphy;K. Murphy;H. Nakajima

c-Maf activates the promoter and enhancer of the IL-21 gene, and TGF- inhibits c-Maf-induced IL-21 production in CD4^+ T cells

c-Maf 激活 IL-21 基因的启动子和增强子，并且 TGF- 抑制 c-Maf 诱导 CD4^ T 细胞中 IL-21 的产生

• 发表时间: 2010
• 期刊: J Leukoc Biol
• 作者: Hiramatsu Y;Suto A;Kashiwakuma D;Hirose K;Watanabe N;Nakajima H;他6名
• 通讯作者: 他6名