Investigation into the roles of autoantibodies in the pathogenesis of central nervous system lupus erythematosus.
Investigation into the roles of autoantibodies in the pathogenesis of central nervous system lupus erythematosus.
批准号:
12670438
负责人:
HIROHATA Shunsei
金额:
$2.18万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2000
资助国家:
日本
项目状态:
已结题
起止时间:
2000 至 2001
中文摘要
我们检测了抗核糖体P蛋白抗体(anti-P)在人免疫能力细胞表面识别的表位的存在,以描述其在中枢神经系统狼疮发病机制中的作用。用亲和纯化的抗p IgG对正常健康人CD4+和GD8+ T细胞、单核细胞和B细胞进行反应,并用fitc偶联的F(ab’)_2山羊抗人IgG片段进行染色,用碘化丙烯染色进行流式细胞术检测活细胞。在新鲜cd4 +和CD8+ T细胞、单核细胞或新鲜B细胞表面未发现与核糖体P蛋白耳甲末端22氨基酸序列具有抗原性相关的表位。然而,核糖体P表位在CD4+和CD8+ T细胞上被固定化抗cd3激活后,在单核细胞上被不含IFN-γ的on孵卵24小时后诱导表达,而在活化的B细胞上不表达。这些结果表明,抗p是一种抗淋巴细胞抗体,可与活化的T细胞和单核细胞发生反应,而不与静止的T细胞、单核细胞或B细胞发生反应,提示抗p可能对系统性红斑狼疮免疫失调有直接作用。狼疮精神病患者脑脊液中抗谷氨酸受体抗体未见明显升高,提示其为抗神经元抗体识别。
英文摘要
We examined the presence of the epitope recognized by antiribosomal P protein antibody (anti-P) on the cell surface of human immunocompetent cells in order to delineate its role in the pathogenesis of CNS lupus. Highly purified CD4+ and GD8+ T cells, monocytes, and B cells from normal healthy individuals were reacted with affinity-purified IgG anti-P, and were stained with FITC-conjugated F(ab')_2, fragment goat anti-human IgG, followed by analysis on flow cytometry with gating for viable cells by propidium iodide staining. The presence of an epitope that is antigenically related to the earboxyl-terminal 22-amino-acid sequence of ribosomal P protein was not demonstrated on the surface offreshCD4+ and CD8+ T cells, monocytes, or fresh B cells. However, the expression of the ribosomal P epitope was induced on CD4+ and CD8+ T cells after activation with immobilized anti-CD3 and on monocytes after 24h incubation with on without IFN-γ, whereas the epitope was not expressed on activated B cells. These results indicate that anti-P is an antilymphocyte' antibody, which reacts with activated T cells and monocytes but not with resting T cells, monocytes or B cells, suggesting possible direct effects of anti-P on the immune dysregulation in systemic lupus erythematosus. We could not detect significant elevation of anti-glutamate receptor antibody in cerebrospinal fluid from patients with lupus psychosis, indicating that recognized by anti-neuronal antibody.
期刊论文(27)
专著(0)
科研奖励(0)
会议论文
登录
查看更多内容
Hirohata S: "Induction of fibroblast-like cells from CD34+ progenitor cells of the bone marrow in rheumatoid arthritis"J.Leukoc.Biol.. 70. 413-421 (2001)
Hirohata S:“类风湿性关节炎中从骨髓 CD34 祖细胞诱导成纤维细胞样细胞”J.Leukoc.Biol.. 70. 413-421 (2001)
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
小嶋浩司: "ポリニューロパチーを合併した抗リン脂質抗体陽性のSLEの1例"日内会誌. 90. 136-137 (2001)
小岛浩二:“抗磷脂抗体阳性 SLE 并发多发性神经病一例”日本学会杂志 90. 136-137 (2001)。
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
広畑俊成: "特集:免疫性神経疾患 -ここまで進んだ病態解明と治療全身性エリテマトーデスに伴う神経障害<その他の自己免疫機序による神経疾患>"内科. 4. 687-691 (2000)
Toshinari Hirohata:“专题:免疫介导的神经系统疾病 - 高级病理学阐明和治疗与系统性红斑狼疮相关的神经病 <由自身免疫机制引起的其他神经系统疾病>”《内科》 4. 687-691 (2000)。
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
広畑俊成: "コンパクト臨床アレルギー学"南江堂. 370 (2000)
Toshinari Hirohata:“紧凑临床过敏学”Nankodo 370 (2000)。
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
Hirohata S: "Bone marrow CD34+ progenitor cells stimulated with stem cell factor and GM-CSF have the capacity to activate IgD-B cells through direct cellular interaction"J.Leukoc.Biology. (in press).
Hirohata S:“用干细胞因子和 GM-CSF 刺激的骨髓 CD34 祖细胞具有通过直接细胞相互作用激活 IgD-B 细胞的能力”J.Leukoc.Biology。
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
共 21 条
Analysis of the mechanism of production of pathologic autoantibodies
-
批准号:23591447
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$3.33万
-
财政年份:2011
-
负责人:HIROHATA Shunsei
-
依托单位:
Analysis of anti-neuronal antibodies in neuropsychiatric systemic lupus erythematosu
-
批准号:20591175
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$3.0万
-
财政年份:2008
-
负责人:HIROHATA Shunsei
-
依托单位:
Molecular analysis of the abnormal expression of CD 154 in T cells as a mechanism of induction of autoinimune disease.
-
批准号:14570431
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$2.24万
-
财政年份:2002
-
负责人:HIROHATA Shunsei
-
依托单位:
Analysis of the molecular machaism of defective T cell functions in reqularing B cell activation in various autoimmune diseases
-
批准号:10670428
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$2.05万
-
财政年份:1998
-
负责人:HIROHATA Shunsei
-
依托单位:
Analysis of the mechanism of abnormal B cell activation characteristic of various autoimmune diseases
-
批准号:06670500
-
项目类别:Grant-in-Aid for General Scientific Research (C)
-
资助金额:$1.41万
-
财政年份:1994
-
负责人:HIROHATA Shunsei
-
依托单位:
Molecular analysis of the abnormal T cell function as a pathogenesis of autoimmune diseases
-
批准号:03807038
-
项目类别:Grant-in-Aid for General Scientific Research (C)
-
资助金额:$1.22万
-
财政年份:1991
-
负责人:HIROHATA Shunsei
-
依托单位:
海外基金