Scholarlink

<p>Psoriasis is a chronic T cell-mediated autoimmune disease characterized by persistent skin inflammation. This study analyzed the GSE47598 dataset from the GEO database to investigate the molecular characteristics of T cells activated in vitro with anti-CD3 and anti-CD28 from peripheral blood mononuclear cells (PBMCs) of psoriasis patients. Gene expression profiling revealed that eukaryotic elongation factor 1 alpha 1 (EEF1A1) was significantly upregulated in activated T cells from psoriasis patients. EEF1A1 was shown to promote the secretion of pro-inflammatory cytokines, including IL-6, IL-22, and TNF-α, contributing to the inflammatory cascade in psoriasis. In an imiquimod-induced mouse model of psoriasis, EEF1A1 expression was markedly elevated in lesional skin and was found to regulate inflammation via the Nuclear factor kappa B (NF-κB) signaling pathway. Targeting EEF1A1 using small interfering RNA (siRNA) reduced inflammatory cytokine levels, highlighting its potential as a therapeutic target. Our findings position EEF1A1 as a potential therapeutic target in psoriasis and warrant further validation in human tissues and in vivo inhibition studies.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

EEF1A1-mediated regulation of inflammatory cytokines in psoriasis: implications for therapeutic strategies

  • 期刊论文

  • 发表日期：

    2025年12月10日

查看全文
  • Huiqin Wang,
  • Yue Du,
  • Yong Liu,
  • Shirong Yu,
  • Weidong Wu

摘要

Psoriasis is a chronic T cell-mediated autoimmune disease characterized by persistent skin inflammation. This study analyzed the GSE47598 dataset from the GEO database to investigate the molecular characteristics of T cells activated in vitro with anti-CD3 and anti-CD28 from peripheral blood mononuclear cells (PBMCs) of psoriasis patients. Gene expression profiling revealed that eukaryotic elongation factor 1 alpha 1 (EEF1A1) was significantly upregulated in activated T cells from psoriasis patients. EEF1A1 was shown to promote the secretion of pro-inflammatory cytokines, including IL-6, IL-22, and TNF-α, contributing to the inflammatory cascade in psoriasis. In an imiquimod-induced mouse model of psoriasis, EEF1A1 expression was markedly elevated in lesional skin and was found to regulate inflammation via the Nuclear factor kappa B (NF-κB) signaling pathway. Targeting EEF1A1 using small interfering RNA (siRNA) reduced inflammatory cytokine levels, highlighting its potential as a therapeutic target. Our findings position EEF1A1 as a potential therapeutic target in psoriasis and warrant further validation in human tissues and in vivo inhibition studies.