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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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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