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Updated: Jun 2, 2025

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在Sjögren干眼病中,S100A8/A9通过调节Acod1/STAT3通路来促进树突细胞介导的Th17细胞反应

Yankai Wei1, Mei Sun1, Xinyu Zhang1

  • 1Tianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, China.

Investigative ophthalmology & visual science
|January 14, 2025
PubMed
概括

斯约格伦干眼病 (SjDED) 涉及S100A8/A9升高,通过Acod1/STAT3通路驱动炎症. 用帕基尼莫德抑制这种途径显示了SjDED的治疗潜力.

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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