ArticleFrontiers in immunology2026
Immune dysregulation and exhaustion in EBV- associated hemophagocytic lymphohistiocytosis: insights from single-cell transcriptomics and TCR repertoire analysis.
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
Introduction: Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis (EBV-HLH) is a life-threatening hyperinflammatory syndrome paradoxically characterized by excessive cytokine production and immune activation despite failure to clear Epstein-Barr virus (EBV). The cellular mechanisms underlying immune dysregulation in EBV-HLH remain incompletely understood. Methods: We performed single-cell RNA sequencing (scRNA-seq) and single-cell T-cell receptor sequencing (scTCR-seq) to characterize the peripheral immune landscape of patients with EBV-HLH. Key findings were validated by flow cytometry and enzyme-linked immunosorbent assay (ELISA) in an independent cohort of 37 patients with secondary hemophagocytic lymphohistiocytosis (sHLH). Results: We identified EBV transcript-positive NK/NKT-like cells undergoing clonal expansion and proliferation as key contributors to immune dysfunction. These cells exhibited high CD160 expression, increased interferon-γ expression, and enrichment of IL-10-mediated signaling. In addition, monocytes acquired an immunosuppressive phenotype characterized by enhanced TGFB1 expression and increased migratory and phagocytic functions. This dysregulated immune environment may promote CD8 Discussion: This study delineates the peripheral immune landscape of EBV-HLH and identifies potential therapeutic targets for EBV-HLH.
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