ArticleBMC gastroenterology2026
Single-cell transcriptomic landscape of intrahepatic B Cells in MASH.
Article in BMC gastroenterology, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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8 authors.
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Abstract
To understand the heterogeneity of single-B cell responses to Metabolic Dysfunction-Associated Steatohepatitis (MASH), we performed Single-cell RNA sequencing (scRNA-seq) on single-B cells isolated from control and MCD-fed mice livers. Subsequent analyses included clustering, identification of differentially expressed genes (DEGs) and enrichment analysis. The expressions of high specific DEGs were validated using quantitative real-time PCR (qRT-PCR), immunofluorescence staining and function study. Four single-B cell clusters (3, 14, 16 and 20) were identified. The total number and proportion of B cells significantly decreased in MASH mice livers. In cluster 3, the decreasing Fcer2α+ mature B cells were supposed with anti-inflammatory role associated with B cell activation and differentiation of other immune cells in MASH. The DEGs (Fcer2α, Cd22, Cr2 and Fcmr) of cluster 3 were consistently downregulated in B cells cocultued with lipotoxic hepatocytes. And the portal area of livers contained fewer Fcer2α+ B cells in MASH patients and mice compared with controls. Fcer2α+ B cells attenuated lipotoxicity-driven inflammation by enhancing anti-inflammatory factor (IL-10, IL-35) secretion and inhibiting T cell inflammatory factor (IFN-γ, TNF-α, IL-17) production and proliferation. The other 3 clusters (14, 16 and 20) contained small numbers of single-B cell. Tnfrsf17+ plasmacytes (PCs) of cluster 14 were identified with the effect related to endoplasmic reticulum stress and N-Glycan biosynthesis. Klk1+ B cells of cluster 16 were implicated in regulating immune response in MASH. Apol7c+ B cells of cluster 20 participated in apoptosis, NF-κB, TNF and JAK-STAT signaling pathway in MASH. Thus, a subgroup of Fcer2α+ mature B cells, diminished in MASH, may exerted anti-inflammatory or immunosuppressive effects.
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