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<p>A20, a negative regulator of NF-κB signaling, is a potent anti-inflammatory molecule. Its deficiency is associated with a wide variety of inflammatory diseases and tumors and the ability of A20 to restrict TCR-NF-<b>κ</b>B signaling pathway and the role of this molecule in the pathogenesis of T-cell leukemia are not completely understood. Here we studied the role of A20 in T cells exposed to staphylococcal enterotoxin A (SEA) and evaluated the results of our <i>in vitro</i> findings of lethal inflammation by long-term administration of SEA at low doses to Jurkat cells, human peripheral blood mononuclear cells, and CD3+ T cells. SEA treatment resulted in chronic inflammation, upregulated the expression of MALT1, IKKβ, and p65, and downregulated the expression of A20, both in dose- and time-dependent manners, in Jurkat cells, regardless of the mRNA or protein level. Thus, SEA-mediated chronic inflammation can activate TCR-NF-κB signals via the downregulation of A20 expression, which increases T-cell immortality and may promote the pathogenesis of T-cell leukemia. Modulation of A20 could be a novel strategy for the treatment of T-cell leukemia.</p>

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Downregulation of A20 Expression Related to T Cells by Staphylococcal Enterotoxin A Treatment

  • 期刊论文

  • 发表日期：

    2025年3月1日

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  • X. Chen,
  • Y. Yan,
  • C. Lin,
  • J. Yang,
  • H. Qiu

摘要

A20, a negative regulator of NF-κB signaling, is a potent anti-inflammatory molecule. Its deficiency is associated with a wide variety of inflammatory diseases and tumors and the ability of A20 to restrict TCR-NF-κB signaling pathway and the role of this molecule in the pathogenesis of T-cell leukemia are not completely understood. Here we studied the role of A20 in T cells exposed to staphylococcal enterotoxin A (SEA) and evaluated the results of our in vitro findings of lethal inflammation by long-term administration of SEA at low doses to Jurkat cells, human peripheral blood mononuclear cells, and CD3+ T cells. SEA treatment resulted in chronic inflammation, upregulated the expression of MALT1, IKKβ, and p65, and downregulated the expression of A20, both in dose- and time-dependent manners, in Jurkat cells, regardless of the mRNA or protein level. Thus, SEA-mediated chronic inflammation can activate TCR-NF-κB signals via the downregulation of A20 expression, which increases T-cell immortality and may promote the pathogenesis of T-cell leukemia. Modulation of A20 could be a novel strategy for the treatment of T-cell leukemia.