ArticleBulletin of experimental biology and medicine2025
Downregulation of A20 Expression Related to T Cells by Staphylococcal Enterotoxin A Treatment.
Article in Bulletin of experimental biology and medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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.
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