Adrb3/IL6 轴在心理社会压力对狼疮发病机制影响中的作用-猫眼课题宝

Adrb3/IL6 轴在心理社会压力对狼疮发病机制影响中的作用

批准号：

10342034

负责人：

Andrew Wang

金额：

$44.46万

依托单位：

YALE UNIVERSITY

依托单位国家：

美国

项目类别：

财政年份：

2022

资助国家：

美国

项目状态：

未结题

起止时间：

2022-02-01 至 2026-12-31

来源：

https://reporter.nih.gov/project-details/10342034

关键词：

Acute Adipocytes Adrenal Glands Adverse effects Agonist Animal Housing Animals Antibodies Antibody Response Autoantibodies Autoimmune Diseases Autoimmunity B-Lymphocytes Biological Biological Assay Body Temperature Brain Catecholamines Cells Chronic Chronic stress Clinical Data Data Development Disease Disease Outcome Event Flare Genetic Glucocorticoids Glucose Goals Helper-Inducer T-Lymphocyte Hepatic Hepatocyte House mice Housing Human IL6 gene Immune Immunity Inflammatory Response Laboratory mice Life Stress Link Lupus Mediating Metabolic Methods Modeling Mus Myeloid Cell Activation Neurons Operative Surgical Procedures Outcome Pathogenesis Pathway interactions Patients Pharmacology Physiologic Thermoregulation Play Production Proteinuria Psychosocial Stress Receptors, Adrenergic, beta-3 Renal function Reporting Role Signal Transduction Source Stress Systemic Lupus Erythematosus Temperature Testing Thermogenesis Translations acute stress antagonist environmental enrichment for laboratory animals fighting genetic approach glucose metabolism hepatic gluconeogenesis immune activation improved insight mortality mouse model novel perceived stress plasma cell differentiation pre-clinical psychosocial psychosocial stressors renal damage response rheumatologist

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中文摘要

翻译

项目摘要已有充分证据表明，心理社会压力与系统性红斑狼疮（SLE）发作相关和SLE预后差。这是如何发生的还没有得到很好的研究。我们最近发现，应激诱导表达Adrb 3的棕色脂肪细胞产生循环IL 6。棕色脂肪细胞来源的IL 6 通过肝脏IL 6信号传导介导免疫代谢重编程，以支持“战斗或逃跑”反应急性压力我们已经得到了初步的数据，慢性心理社会压力可能会增加死亡率，通过这种新的Adrb 3/IL 6途径在SLE小鼠模型中的作用。在这里，我们建议剖析 Adrb 3/IL 6通路在心理社会应激对SLE发病机制的影响除了为了从生物学上了解心理社会压力如何导致狼疮免疫激活增加，我们研究将为潜在的人类翻译提供令人信服的临床前数据。

英文摘要

PROJECT SUMMARY Psychosocial stress has been well-documented to correlate with systemic lupus erythematosus (SLE) flares and poor SLE outcomes. How this occurs has not been well studied. We recently identified that psychosocial stress induces circulating IL6 produced by Adrb3-expressing brown adipocytes. Brown adipocyte-derived IL6 mediates immunometabolic reprogramming through hepatic IL6 signaling to support “fight or flight” responses to acute stress. We have generated preliminary data that chronic psychosocial stress may enhance mortality in murine models of SLE through this novel Adrb3/IL6 pathway. Here, we propose to dissect the role of the Adrb3/IL6 pathway in the impact of psychosocial stress on SLE pathogenesis in murine models. In addition to gaining biological insight into how psychosocial stress leads to increased immune activation in lupus, our studies would provide compelling pre-clinical data for potential human translation.

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