Modulation of Autoantigen Trafficking and TLR engagement by FcgRIIB and AP3B1

FcgRIIB 和 AP3B1 对自身抗原运输和 TLR 参与的调节

• 批准号: 8521057
• 负责人: Krishna-sulayman Laroche Moody
• 金额: $ 2.96万
• 依托单位: BOSTON UNIVERSITY MEDICAL CAMPUS
• 依托单位国家: 美国
• 财政年份: 2012
• 资助国家: 美国
• 起止时间: 2012-08-01 至 2015-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8521057
• 关键词: Actins; Adaptor Protein Complex 3; Affect; Antibodies; Antigen-Antibody Complex; Attention; Autoantibodies; Autoantigens; Autoimmune Diseases; Autoimmune Process; Autoimmunity; B Cell Proliferation; B-Lymphocytes; Binding; Cells; Clinical; Complex; Confocal Microscopy; Cytoskeletal Modeling; DNA; Data; Defect; Dendritic Cells; Development; Disease; Effector Cell; Environment; Exhibits; Flow Cytometry; Genetic; Goals; Human; Immune; Immune Cell Activation; Immunoglobulin G; In Vitro; Interferon Type I; Interferons; Interleukin-6; Laboratories; Ligands; Lupus; Mediating; Modeling; Molecular; Monitor; Mus; Myelogenous; Nucleic Acids; Outcome; Pathogenesis; Patients; Pattern; Phagocytes; Phase II Clinical Trials; Phosphorylation; Process; Production; Proliferating; Public Health; RANTES; RNA; Resistance; Ribonucleases; Role; Signal Transduction; Susceptibility Gene; TLR7 gene; TNF gene; Testing; Therapeutic Agents; cytokine; functional outcomes; in vivo Model; inhibitor/antagonist; mouse model; novel; public health relevance; response; sensor; systemic autoimmune disease; trafficking

DESCRIPTION (provided by applicant): Our lab is focused on understanding how pathogenic immune complexes (IC) formed from DNA and/or RNA and antibodies contribute to the pathogenesis of systemic lupus erythematous (SLE). We use in vitro and in vivo models to determine the molecular mechanisms that govern the activation of immune cells by DNA and/or RNA antibody complexes. This particular project is investigating how IC trafficking within immune cells affects the functional outcome. We have developed novel ICs that are also pH sensors. Using these ICs we can rapidly screen the effect of genetic factors and therapeutic agents on IC trafficking in B cells and phagocytes.

描述（由申请人提供）：我们的实验室专注于了解由DNA和/或RNA和抗体形成的致病性免疫复合物（IC）如何促进系统性红斑狼疮（SLE）的发病机制。我们使用体外和体内模型来确定DNA和/或RNA抗体复合物激活免疫细胞的分子机制。这个特别的项目正在研究免疫细胞内的IC运输如何影响功能结果。我们开发了新型的IC，也是pH传感器。利用这些IC，我们可以快速筛选遗传因素和治疗剂对IC在B细胞和吞噬细胞中运输的影响。