SLAM Gene Family Controlled Pathways to SLE

SLAM 基因家族控制 SLE 通路

• 批准号: 8513250
• 负责人: CORNELIS P TERHORST
• 金额: $ 151.41万
• 依托单位: BETH ISRAEL DEACONESS MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-08-15 至 2017-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8513250
• 关键词: Address; Adhesions; Advisory Committees; Affect; Alleles; Alternative Splicing; Amino Acid Sequence; Amino Acids; Antibody Avidity; Antigen Presentation; Apoptosis; Arthralgia; Autoantibodies; Autoimmune Diseases; Autoimmune Process; Autoimmunity; B-Lymphocytes; Basic Science; Binding; Binding Sites; Biological Markers; CD28 gene; CD3 Antigens; CD4 Positive T Lymphocytes; CD44 gene; Cell Communication; Cell physiology; Cell surface; Cells; Chromosomes, Human, Pair 1; Chronic; Clinical; Code; Complement; Complementary DNA; Complex; Congenic Mice; Cytoplasmic Tail; Data; Dendritic Cells; Diagnostic; Disease; Disease susceptibility; Event; Exanthema; Fatigue; Female of child bearing age; Funding; Gene Family; Gene Transfer Techniques; Genes; Genetic; Genetic Engineering; Genetic Polymorphism; Goals; Haplotypes; Hereditary Disease; Human; Immune; Immune response; Immunity; Immunobiology; Immunoglobulin G; Immunologic Receptors; Immunosuppressive Agents; Inbred BALB C Mice; Individual; Infection; Institution; Interleukin-17; Interleukin-2; Investigation; Israel; Kidney; Knockout Mice; Lead; Leadership; Ligands; Lupus; Medical; Medical center; Membrane; Microbiology; Molecular; Monitor; Monoclonal Antibodies; Mononuclear; Mouse Strains; Mus; Nephritis; Nuclear; Outcome; Outcome Study; Pathogenesis; Pathology; Pathway interactions; Patients; Phagocytes; Pharmaceutical Preparations; Phenotype; Phosphorylation; Play; Production; Productivity; Progress Reports; Property; Protein Isoforms; Reaction; Receptor Gene; Refuse Disposal; Reporting; Research; Research Personnel; Role; SLAM family receptor; Signal Transduction; Spliced Genes; Strategic Planning; Surface; Surface Antigens; Synapses; System; Systemic Lupus Erythematosus; T-Lymphocyte; T-Lymphocyte Subsets; Testing; Therapeutic; To autoantigen; Transgenes; Transgenic Organisms; Translational Research; Treatment Protocols; Tyrosine; Variant; Work; X Chromosome; base; cytokine; disorder risk; human disease; indexing; innovation; insight; medical schools; member; memory CD4 T lymphocyte; microbial; mouse model; novel; programs; promoter; receptor; research study; sensor; src Homology Region 2 Domain; tool

DESCRIPTION (provided by applicant): This application seeks support for elucidating the role of the SLAMF receptors in the pathogenesis of Systemic Lupus Erythematosus (SLE) with the ultimate goal to develop SLAMF-based therapeutic strategies that can be applied to SLE patients. Because of the outcomes of our studies with cells derived from SLE patients and our exciting findings with genetically altered mice, which develop lupus-related autoimmunity, we now have the systems in place to dissect how cell interaction mechanisms and signaling initiated by the SLAMF receptors contribute to the control of tolerance to autoantigens and to the pathogenesis of human SLE. These insights and tools are the basis for a Program Project application entitled: "SLAM FAMILY RECEPTOR CONTROLLED PATHWAYS TO SLE" for three interlinked projects and two supporting Cores. Project #1 The SlamfS, Slamf5 and Slamf6 receptor-induced pathways to murine lupus. PL: Cox Terhorst, Beth Israel Deaconess Medical Center. Project #2 Functional analyses of human and mouse SLAMF4"SLAMF2 receptor / ligand interactions in murine and human SLE. PL: Arlene Sharpe, Department of Microbiology and Immunobiology, Harvard Medical School. Project #3 Function of human SLAMF receptors in SLE immune cells. PL: George Tsokos, Beth Israel Deaconess Medical Center. Core A Genetic Mouse Core.PL: Ninghai Wang, Beth Israel Deaconess Medical. Center Core B Administrative Core.PL Cox Terhorst, Beth Israel Deaconess Medical Center.

描述（由申请人提供）：