ReviewFrontiers in immunology2026
Spatial immune dysregulation in MASLD: integration of lobular zoning, metabolism and immune function.
Review 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
Most prior studies on immune-related fatty liver disease have focused on changes in immune cell quantity and composition. However, this "cell-count model" does not fully explain the regional onset of fibrosis, spatial heterogeneity of lesions, or variable immunotherapy responses. Immune dysregulation in metabolic dysfunction-associated steatotic liver disease (MASLD) involves not only compositional changes but also spatial redistribution and functional alterations of immune cells within specific hepatic lobule regions. Emerging multi-omics and spatial transcriptomic data suggest that chemokine gradient remodeling, metabolic microenvironment reprogramming, and circadian rhythm disruption may drive immune cell relocation along the portal-central axis. We propose that immune dysregulation in MASLD reflects a disruption of spatial immune homeostasis and introduce the liver lobule as the basic unit for spatial immune analysis. The lobule comprises three functionally distinct zones: the periportal zone (zone 1), which serves as the primary immune surveillance barrier; the pericentral zone (zone 3), characterized by metabolic stress and functional impairment; and the fibrotic septum, which in advanced disease creates a structurally confined immunosuppressive niche. To quantify regional T cell dysfunction, we propose a Regional Exhaustion Index (REI) as a conceptual framework, calculated as the ratio of PD-1
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