SEARCH FOR NOVEL B CELL HYPERACTIVITY GENES
SEARCH FOR NOVEL B CELL HYPERACTIVITY GENES
批准号:
6100391
负责人:
SYAMAL K DATTA
金额:
$15.9万
依托单位国家:
美国
项目类别:
财政年份:
1998
资助国家:
美国
项目状态:
已结题
起止时间:
1998-12-01 至 1999-11-30
关键词:
B lymphocyte CD5 molecule animal genetic material tag apoptosis biological signal transduction cell differentiation complementary DNA flow cytometry gene expression genetic strain immunogenetics laboratory mouse leukocyte activation /transformation messenger RNA molecular cloning northern blottings nucleic acid sequence polymerase chain reaction receptor expression systemic lupus erythematosus
中文摘要
我们的长期目标是识别出那些
确定B细胞,特别是B-1(DC 5-谱系)B的过度活性
细胞 新西兰黑(NZB)小鼠,具有终身
将研究过度活跃的ob B-1细胞。 NZB小鼠不仅
发展自身免疫性疾病,而且恶性发病率高,
与人CLL非常相似的B-1 B细胞的淋巴瘤,
艾滋病患者发生的B细胞淋巴瘤。 此外,B-1 B
类风湿性关节炎(RA)的炎症关节中的细胞过度活跃
在抗原呈递中起主要作用的患者,
激活炎症细胞。 我们有初步证据
显示NZ B小鼠的过度活跃的B细胞差异表达
在正常B细胞中不表达的几种基因。 在这
发展和可行性研究,我们想确认,
这些B细胞过度活跃基因的同一性。 最终我们的目标是
克隆这些差异表达基因的全长cDNA,
对它们进行测序,研究它们的基因组结构,
功能 对B细胞过度活跃基因的研究可能揭示新的
基因或已知基因的新功能 除了与RA相关外,
和恶性B细胞淋巴瘤如上所述,该项目可以
提高我们对B细胞的基本机制的认识
分化、信号转导、耐受和凋亡。
英文摘要
Our long-term goal is to identify the genes and their products that
determine hyperactivity of B cells, particularly B-1 (DC5-lineage) B
cells. New Zealand Black (NZB) mice, that have a life-long
hyperactivity ob B-1 cells, will be studied. NZB mice not only
develop autoimmune disease but also a high incidence of malignant
lymphomas of B-1 B cells that are very similar to human CLL and the
B cell lymphomas developing the AIDS patients. In addition B-1 B
cells are hyperactive in the inflamed joints of rheumatoid arthritis (RA)
patients where they play a major role in antigen presentation and
activation of inflammatory cells. We have preliminary evidence
showing that the hyperactive B cells of NZB mice differentially express
several genes that are not expressed in normal B cells. In this
development and feasibility study, we would like to confirm the
identity of these B cell hyperactivity genes. Eventually we aim to
clone the full length cDNA for these differentially expressed genes,
sequence them, study their genomic organization and define their
function. This search for B cell hyperactivity genes may reveal novel
genes or new function for known genes. Besides its relevance to RA
and malignant B cell lymphomas as stated above, this project could
enhance our understanding of the basic mechanisms of B cell
differentiation, signal transduction, tolerance and apoptosis.
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IMMUNE MECHANISMS OF ANTICD40L TRIAL IN SLE
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批准号:2882256
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项目类别:
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资助金额:$22.46万
-
财政年份:1999
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负责人:SYAMAL K DATTA
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依托单位:
IMMUNE MECHANISMS OF ANTICD40L TRIAL IN SLE
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批准号:6137339
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项目类别:
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资助金额:$22.3万
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财政年份:1999
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依托单位:
IMMUNE MECHANISMS OF ANTICD40L TRIAL IN SLE
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批准号:6341792
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项目类别:
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资助金额:$22.83万
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财政年份:1999
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负责人:SYAMAL K DATTA
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批准号:6268330
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资助金额:$15.61万
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财政年份:1997
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项目类别:
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资助金额:$17.17万
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财政年份:1993
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负责人:SYAMAL K DATTA
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依托单位:
MECHANISM OF AUTOIMMUNE RESPONSE IN HUMAN LUPUS
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批准号:2457949
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项目类别:
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资助金额:$16.51万
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财政年份:1993
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负责人:SYAMAL K DATTA
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依托单位:
MECHANISM OF AUTOIMMUNE RESPONSE IN HUMAN LUPUS
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批准号:6043194
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项目类别:
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资助金额:$17.86万
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财政年份:1993
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负责人:SYAMAL K DATTA
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依托单位:
MECHANISM OF AUTOIMMUNE RESPONSE IN HUMAN LUPUS
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批准号:6374902
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项目类别:
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资助金额:$28.52万
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财政年份:1993
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负责人:SYAMAL K DATTA
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依托单位:
MECHANISM OF AUTOIMMUNE RESPONSE IN HUMAN LUPUS
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批准号:2079421
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项目类别:
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资助金额:$15.88万
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财政年份:1993
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负责人:SYAMAL K DATTA
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依托单位:
MECHANISM OF AUTOIMMUNE RESPONSE IN HUMAN LUPUS
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批准号:6651197
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项目类别:
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资助金额:$28.52万
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财政年份:1993
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负责人:SYAMAL K DATTA
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项目类别:
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资助金额:$28.52万
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财政年份:1993
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负责人:SYAMAL K DATTA
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依托单位:
PATHOGENIC ANTIDNA AUTOANTIAB REGULATION IN LUPUS
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批准号:2079420
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项目类别:
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资助金额:$13.19万
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财政年份:1993
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负责人:SYAMAL K DATTA
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依托单位:
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批准号:6786632
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项目类别:
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资助金额:$28.52万
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财政年份:1993
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负责人:SYAMAL K DATTA
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依托单位:
MECHANISM OF AUTOIMMUNE RESPONSE IN HUMAN LUPUS
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项目类别:
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资助金额:$29.7万
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财政年份:1993
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负责人:SYAMAL K DATTA
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依托单位:
MECHANISM OF AUTOIMMUNE RESPONSE IN HUMAN LUPUS
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项目类别:
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资助金额:$29.0万
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财政年份:1993
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负责人:SYAMAL K DATTA
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依托单位:
MECHANISM OF AUTOIMMUNE RESPONSE IN HUMAN LUPUS
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项目类别:
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资助金额:$28.16万
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财政年份:1993
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负责人:SYAMAL K DATTA
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项目类别:
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资助金额:$28.52万
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财政年份:1993
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负责人:SYAMAL K DATTA
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项目类别:
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资助金额:$27.6万
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财政年份:1993
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负责人:SYAMAL K DATTA
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资助金额:$12.66万
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财政年份:1993
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依托单位:
海外基金