Identification of Hepatic Dendritic Cells in Liver Biopsies in Patients with Metabolic Dysfunction-Associated Fatty Liver Diseas (MAFLD) and Obesity

Background: Metabolic dysfunction-associated fatty liver disease (MAFLD) is now the term used for hepatic steatosis in pa-tients who are overweight or obese, have type 2 diabetes mellitus (T2DM), or evidence of metabolic dysregu-lation. The prevalence of MAFLD among morbidly obese subjects is 65-93%. Hepatic dendritic cells (hDCs) are antigen-presenting cells that induce T cell-mediated immunity. MAFLD pathogenesis involves numerous im-mune cell-mediated inflammatory processes, while the particular role of hDCs is yet to be well defined. This study aimed to identify hDCs in liver biopsies from 128 patients with MAFLD associated with obesity. Material/Methods: In this cross-sectional study, 128 liver biopsies from 128 patients with MAFLD (diagnosed as presence of he-patic steatosis, plus T2DM, metabolic dysregulation or overweight/obesity) were collected and assessed for CD11c+ immunoreactivity degree (CD11c as dendritic cell biomarker), through antigen retrieval, reaction with CD11c antibodies (primary), and marking with diaminobenzidine chromogen. Results: Among the 128 patients with MAFLD, 64 (50%) had MAFLD and fibrosis and 72 (56.2%) positively expressed hDCs (CD11c+). Among morbidly obese patients, 49 (64.5%) positively expressed hDCs (CD11c+) in liver tissue; from patients with obesity grade I-grade II (GI-II), 18 (54.5%) positively expressed hDCs (CD11c+) in liver tis-sue; and from non-obese patients with MAFLD, 5 (26.3%) positively expressed hDCs (CD11c+) in liver tissue. Conclusions: hDC expression increases significantly in morbidly obese patients with MAFLD compared with non-obese pa-tients, independent of the degree of fibrosis, suggesting the role of adaptive changes within hDCs in the per-petuation of inflammatory insults in chronic liver diseases.

Automated summary

This study identified increased expression of hDCs in MAFLD patients, independent of the degree of obesity. This suggests the role of adaptive changes within hDCs in perpetuating inflammatory insults in chronic liver diseases.