树突状细胞中Blimp1/prdm-1在自身抗体生成中的功能-猫眼课题宝

树突状细胞中Blimp1/prdm-1在自身抗体生成中的功能

批准号：

8683106

负责人：

Sun Jung Kim

金额：

$5.72万

依托单位：

FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH

依托单位国家：

美国

项目类别：

财政年份：

2010

资助国家：

美国

项目状态：

已结题

起止时间：

2010-07-02 至 2015-06-30

来源：

https://reporter.nih.gov/project-details/8683106

关键词：

Ablation Adoptive Transfer Affect Age-Months Antibodies Autoantibodies Autoimmune Diseases Autoimmunity B-Lymphocytes Belief Blood Bone Marrow CD4 Positive T Lymphocytes Cell physiology Cells Cellular biology Cessation of life Clinic Clinical Data Dendritic Cells Development Disease Effector Cell Estradiol Estrogens Exhibits Female Frequencies Generations Helper-Inducer T-Lymphocyte ITGAX gene Immune Immune Tolerance Immune system Immunoglobulin G Immunoglobulin M Implant In Vitro Inflammation Inflammatory Injury Lead Lupus Measures Mediating Modeling Mus Mutation Nuclear Organ Pattern Phagocytosis Phenotype Placebos Production Regulation Role Serologic tests Serum Somatic Mutation Spleen Splenomegaly Structure of germinal center of lymph node Systemic Lupus Erythematosus T-Lymphocyte Testing Tissues Toll-like receptors Weight Wild Type Mouse Woman autoreactive B cell autoreactivity cytokine human disease immune activation in vivo lupus-like male men new therapeutic target novel precursor cell prevent response

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DESCRIPTION (provided by applicant): Systemic Lupus (SLE) is an autoimmune disease characterized by the production of an array of anti- nuclear antibodies that affects women far more frequently than men. Abnormal B and T cell function has been extensively studied in murine models of SLE. We have developed a mouse with a deletion of Blimp-1 function uniquely in dendritic cells. Female mice develop a lupus-like serology while male mice do not. We propose to understand the alterations in dendritic cell function and the mechanism for the subsequent dysregulation of B cell function. Furthermore, we will determine why this genetic defect manifests as autoimmunity only in female mice. These studies will further our understanding of dendritic cell biology and may identify a new therapeutic target in SLE.

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