Role of B Lymphocytes in the Pathogenesis of NAFLD: A 2022 Update

Deng, Chujun; Lo, Tak-Ho; Chan, Ka-Ying; Li, Xiang; Zou, Xiang; Wong, Chi Ming

doi:10.3390/ijms232012376

Cited by 14 publications

(5 citation statements)

References 80 publications

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“…MSCs can also reverse the fibrosis process and lobular inflammatory infiltration in MAFLD mice induced by high-fat diet (HDF) by inhibiting CD4+ T cell proliferation [18]. B cells can mediate liver injury and fibrosis and further promote the development of NASH to fibrosis [56]. Corcione et al [57] found that MSCs may secrete soluble factors through paracrine pathway to arrest the cell cycle of B cells in G0/G1 and inhibit the proliferation of B cells.…”

Section: Immunomodulatory Effect Of Mscsmentioning

confidence: 99%

Mechanisms of Action of Mesenchymal Stem Cells in Metabolic-Associated Fatty Liver Disease

Cong

Zhu

et al. 2023

Stem Cells International

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Metabolic-associated fatty liver disease (MAFLD) is currently the most common chronic liver disease worldwide. However, its pathophysiological mechanism is complicated, and currently, it has no FDA-approved pharmacological therapies. In recent years, mesenchymal stem cell (MSC) therapy has attracted increasing attention in the treatment of hepatic diseases. MSCs are multipotent stromal cells that originated from mesoderm mesenchyme, which have self-renewal and multipotent differentiation capability. Recent experiments and studies have found that MSCs have the latent capacity to be used for MAFLD treatment. MSCs have the potential to differentiate into hepatocytes, which could be induced into hepatocyte-like cells (HLCs) with liver-specific morphology and function under appropriate conditions to promote liver tissue regeneration. They can also reduce liver tissue injury and reverse the development of MAFLD by regulating immune response, antifibrotic activities, and lipid metabolism. Moreover, several advantages are attributed to MSC-derived exosomes (MSC-exosomes), such as targeted delivery, reliable reparability, and poor immunogenicity. After entering the target cells, MSC-exosomes help regulate cell function and signal transduction; thus, it is expected to become an emerging treatment for MAFLD. In this review, we comprehensively discussed the roles of MSCs in MAFLD, main signaling pathways of MSCs that affect MAFLD, and mechanisms of MSC-exosomes on MAFLD.

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Section: Immunomodulatory Effect Of Mscsmentioning

confidence: 99%

Mechanisms of Action of Mesenchymal Stem Cells in Metabolic-Associated Fatty Liver Disease

Cong

Zhu

et al. 2023

Stem Cells International

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“…190,191 Chronic inflammation is central to NAFLD disease progression and involves both residential and circulating immune cells, including macrophages and lymphocytes. 192,193 The interaction between the different cell types also involves a slew of inflammatory chemokines and cytokines, such as chemokine (C-C motif) ligand 2 (CCL-2), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), interleukin-17 (IL-17), and interleukin-18 (IL-18). [194][195][196][197] The treatment of fatty liver disease currently consists of lifestyle recommendations, including regulating calorie intake and exercise.…”

Section: Nonalcoholic Fatty Liver Disease (Nafld)mentioning

confidence: 99%

“…In addition, gut microbes have been reported to be involved in the development of NAFLD via the regulation of bile acid metabolism, lipid handling, and endotoxin and metabolite production in the gut [ 165 , 166 ]. Chronic inflammation is central to NAFLD disease progression and involves both residential and circulating immune cells, including macrophages and lymphocytes [ 167 , 168 ]. Interactions among the different cell types also involve a slew of inflammatory chemokines and cytokines, such as chemokine ligand 2, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), IL-1β, IL-17, and IL-18 [ 169 - 172 ].…”

Section: Nonalcoholic Fatty Liver Diseasementioning

confidence: 99%

A decade of liver organoids: Advances in disease modeling

Liu¹,

Sheng²,

Ding³

et al. 2023

Clin Mol Hepatol

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Liver organoids are 3D cellular models of tissue in which cells interact to form unique structures in culture. Since their inception, liver organoids with various cellular compositions, structural features, and functional properties have been described over the past ten years. Methods to create these advanced human cell models range from simple tissue culture techniques to complex bioengineering approaches. These liver organoid culture platforms have been utilized in various liver research fields, including the modeling of liver diseases to regenerative therapy. This review will discuss how liver organoids are used to model diseases, including hereditary liver diseases, primary liver cancer, viral hepatitis, and nonalcoholic fatty liver disease. Specifically, we will focus on studies that utilized two widely adopted approaches: differentiation from pluripotent stem cells and epithelial organoids cultured from patient tissues. These approaches have enabled the generation of advanced human liver models and, more importantly, the establishment of patient-tailored models for evaluating individual-specific disease phenotypes and therapeutic responses.

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“…For example, the ratios of regulatory T cells (Tregs) with T helper 1 (Th1) cells, Th17, and CD8 T cells are increased in the pathogenesis of NAFLD, NASH, fibrosis, and NASH-associated HCC [16,131]. Recent studies have also demonstrated that CD4 -CD8double negative T cells make an important contribution to NAFLD and NASH [132,133]. B cells play dual roles in diet-induced NAFLD by secreting cytokines and antibodies, a phenomenon that was reviewed in a recent literature report [134].…”

Section: Inflammation Of Liver Innate and Adaptive Immune Cellsmentioning

confidence: 99%

Molecular mechanisms of metabolic disease-associated hepatic inflammation in non-alcoholic fatty liver disease and non-alcoholic steatohepatitis

Zhang,

Sui,

Liu

et al. 2023

Explor Dig Dis

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Non-alcoholic fatty liver disease (NAFLD) is the leading chronic liver disease worldwide, with a progressive form of non-alcoholic steatohepatitis (NASH). It may progress to advanced liver diseases, including liver fibrosis, cirrhosis, and hepatocellular carcinoma. NAFLD/NASH is a comorbidity of many metabolic disorders such as obesity, insulin resistance, type 2 diabetes, cardiovascular disease, and chronic kidney disease. These metabolic diseases are often accompanied by systemic or extrahepatic inflammation, which plays an important role in the pathogenesis and treatment of NAFLD or NASH. Metabolites, such as short-chain fatty acids, impact the function, inflammation, and death of hepatocytes, the primary parenchymal cells in the liver tissue. Cholangiocytes, the epithelial cells that line the bile ducts, can differentiate into proliferative hepatocytes in chronic liver injury. In addition, hepatic non-parenchymal cells, including liver sinusoidal endothelial cells, hepatic stellate cells, and innate and adaptive immune cells, are involved in liver inflammation. Proteins such as fibroblast growth factors, acetyl-coenzyme A carboxylases, and nuclear factor erythroid 2-related factor 2 are involved in liver metabolism and inflammation, which are potential targets for NASH treatment. This review focuses on the effects of metabolic disease-induced extrahepatic inflammation, liver inflammation, and the cellular and molecular mechanisms of liver metabolism on the development and progression of NAFLD and NASH, as well as the associated treatments.

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Role of B Lymphocytes in the Pathogenesis of NAFLD: A 2022 Update

Cited by 14 publications

References 80 publications

Mechanisms of Action of Mesenchymal Stem Cells in Metabolic-Associated Fatty Liver Disease

Mechanisms of Action of Mesenchymal Stem Cells in Metabolic-Associated Fatty Liver Disease

A decade of liver organoids: Advances in disease modeling

Molecular mechanisms of metabolic disease-associated hepatic inflammation in non-alcoholic fatty liver disease and non-alcoholic steatohepatitis

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