ArticleFrontiers in immunology2026
Nuclear localization of Toll/interleukin-1 receptor domain-containing adaptor protein reveals a previously unrecognized role in hepatic stellate cell activation.
Article in Frontiers in immunology, 2026. 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
Background: The Toll/interleukin-1 receptor domain-containing adaptor protein (TIRAP) is a key adaptor in Toll-like receptor signaling, classically functioning as a cytoplasmic bridging adaptor for Myeloid differentiation primary response 88 (MyD88) recruitment. While its role in inflammatory signaling is well established, its contribution to alcohol-induced liver fibrosis remains unclear. Methods: We used lipopolysaccharide (LPS) and ethanol-stimulated hepatic stellate cells (LX-2) for Results: We demonstrated for the first time, nuclear translocation of TIRAP under alcoholic conditions. Confocal microscopy and nuclear-cytoplasmic fractionation confirmed TIRAP enrichment in the nucleus. Importantly, silencing of TIRAP in LX-2 significantly reduced the nuclear translocation and expression of fibrotic markers (such as Conclusion: Overall, these findings reveal a novel role for TIRAP beyond cytoplasmic signaling, suggesting potential nuclear functions that may regulate transcriptional programs driving inflammation and fibrosis.
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