Suppressors of Cytokine Signalling (SOCS) have Neuroprotective Roles in Retina

细胞因子信号传导抑制剂 (SOCS) 对视网膜具有神经保护作用

• 批准号: 10706095
• 负责人: Charles E Egwuagu
• 金额: $ 14万
• 依托单位: NATIONAL EYE INSTITUTE
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10706095
• 关键词: B-Lymphocytes; CISH gene; Cell Proliferation; Cells; Cessation of life; Cytokine Signaling; Disease; Embryonic Development; Eye; Insecta; Interferons; Lymphocyte; Mammals; Mediating; Mus; Mutant Strains Mice; PTPN6 gene; Pathogenicity; Pathologic; Pathway interactions; Physarum polycephalum; Physiological Processes; Proteins; Regulation; Research; Retina; Role; STAT3 gene; Signal Transduction; Uveitis; autoimmune uveitis; in vivo; peptidomimetics; transcription factor

Alterations in in vivo levels of SOCS3 or SOCS1 was previously shown to influence immunopathogenic mechanisms that mediate uveitis. We have also shown that SOCS3 mimetic peptides is effective in suppressing experimental autoimmune uveitis. In our current study, we show that perturbation of SOCS3 levels in mice with STAT3 deficiency in B cells exacerbated uveitis by promoting expansion of pathogenic lymphocytes. We will continue to use mutant mice with alterations of JAK/STAT signaling to further elucidate the role of SOCS1 and SOCS3 in ocular diseases.

先前表明 SOCS3 或 SOCS1 体内水平的改变会影响介导葡萄膜炎的免疫致病机制。我们还表明 SOCS3 模拟肽可有效抑制实验性自身免疫性葡萄膜炎。在我们目前的研究中，我们发现，B 细胞中 STAT3 缺陷的小鼠中 SOCS3 水平的扰动会通过促进致病性淋巴细胞的扩张而加剧葡萄膜炎。 我们将继续使用 JAK/STAT 信号改变的突变小鼠来进一步阐明 SOCS1 和 SOCS3 在眼部疾病中的作用。