Transcriptional network analysis implicates altered hepatic immune function in NASH development and resolution
Open accessAbstract
Progression of fatty liver to non-alcoholic steatohepatitis (NASH) is a rapidly growing health problem. Presence of inflammatory infiltrates in the liver and hepatocyte damage distinguish NASH from simple steatosis. However, the underlying molecular mechanisms involved in the development of NASH remain to be fully understood. Here we perform transcriptional and immune profiling of NASH patients before and after lifestyle intervention (LSI). Analysis of liver microarray data from a cohort of patients with histologically assessed NAFLD reveals a hepatic gene signature, which is associated with NASH and is sensitive to regression of NASH activity upon LSI independently of body weight loss. Enrichment analysis reveals the presence of immune-associated genes linked to inflammatory responses, antigen presentation and cytotoxic cells in the NASH-linked gene signature. In an independent cohort, NASH is also associated with alterations in blood immune cell populations, including conventional dendritic cells (cDC) type 1 and 2, and cytotoxic CD8 T cells. Lobular inflammation and ballooning are associated with the accumulation of CD8 T cells in the liver. Progression from simple steatosis to NASH in a mouse model of diet-driven NASH results in a comparable immune-related hepatic expression signature and the accumulation of intra-hepatic cDC and CD8 T cells. These results show that NASH, compared to normal liver or simple steatosis, is associated with a distinct hepatic immune-related gene signature, elevated hepatic CD8 T cells, and altered antigen-presenting and cytotoxic cells in blood. These findings expand our understanding of NASH and may identify potential targets for NASH therapy.
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The S100hiHLAlo cDC2 (mregDC) subset is enriched in the liver with MASLD/MASH progression measurements.
“The S100hiHLAlo cDC2 (mregDC) subset was also enriched in the liver with MASLD/MASH progression measurements (Fig. 4g)”
From Single-cell atlas of human liver and blood immune cells across fatty liver disease stages reveals distinct signatures linked to liver dysfunction and fibrogenesis (2025) · cites this paper as [31]
The Results section, “Diet-induced NASH drives increased liver cDC2 and CD8 T cells” (page unavailable), reports increased CD172a+ cDC resembling human cDC2 in mouse livers after NASH induction. The paper also associates circulating human cDC2 with NASH activity, but it does not identify an S100hiHLAlo cDC2 (mregDC) subset or demonstrate that this specific subset is enriched in human liver with disease progression. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe HLAhiS100lo cDC2 and S100hiHLAlo cDC2 subsets tend to increase with liver fibrosis measurements in the periphery.
“The HLAhiS100lo cDC2 and S100hiHLAlo cDC2 subsets, in contrast, tended to increase with liver fibrosis measurements in the periphery (Fig. 4g)”
From Single-cell atlas of human liver and blood immune cells across fatty liver disease stages reveals distinct signatures linked to liver dysfunction and fibrogenesis (2025) · cites this paper as [31]
The Results section, “Blood immune cells signatures of NASH” (page unavailable), reports that circulating cDC2-like cells positively correlated with NASH activity. It does not distinguish HLAhiS100lo from S100hiHLAlo cDC2 or report that either subset increases with liver fibrosis measurements. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe frequency of XCR1+ cDC1s decreases with liver fibrosis measurements (histological fibrosis stages, APRI, FIB-4, and liver stiffness) in both liver and peripheral blood.
“revealed a decrease in the frequency of XCR1+ cDC1s with liver fibrosis measurements (histological fibrosis stages, APRI, FIB-4 and liver stiffness) in the liver and peripheral blood (Fig. 4g)”
From Single-cell atlas of human liver and blood immune cells across fatty liver disease stages reveals distinct signatures linked to liver dysfunction and fibrogenesis (2025) · cites this paper as [31]
The Results section on diet-induced NASH reports fewer hepatic XCR1+ cDC1s in mice, while the blood-immune-cell Results and Discussion report an inverse association between circulating cDC1s and NASH activity in humans. The paper does not establish the claimed decrease against histological fibrosis stage, APRI, FIB-4, or liver stiffness in both liver and blood; its liver and blood findings also come from different species. (LLM, conf=0.87)
Experimental — accuracy not yet measuredWithin the MASLD/MASH spectrum, peripheral blood XCR1+ cDC1 frequency decreases with disease progression.
“yet, when assessed within the MASLD/MASH spectrum, they were found to decrease with disease progression31, as in our data.”
From Single-cell atlas of human liver and blood immune cells across fatty liver disease stages reveals distinct signatures linked to liver dysfunction and fibrogenesis (2025) · cites this paper as [31]
The Results (‘Blood immune cells signatures of NASH’; page not provided) report that circulating CD141+ cDC1 are inversely correlated with NASH activity. The Results (‘Diet-induced NASH drives increased liver cDC2 and CD8 T cells’; page not provided) identify the decreased XCR1+ cDC population in mouse liver, not human peripheral blood. The paper therefore supports the blood cDC1 trend but not the specific claim about peripheral-blood XCR1+ cDC1. (LLM, conf=0.87)
Experimental — accuracy not yet measuredThe study delineated a fibrosis-related enrichment of CD8+ TEM cells harboring an exhausted signature in the liver, whereas CD8+ TEMRA cell frequency increased in peripheral blood with liver steatosis as assessed by CAP.
“We delineated a fibrosis-related enrichment of CD8+ TEM cells harboring a previously reported exhausted signature31,34,35 in the liver, whereas the frequency of CD8+ TEMRA cells increased in the peripheral blood with liver steatosis as assessed by CAP”
From Single-cell atlas of human liver and blood immune cells across fatty liver disease stages reveals distinct signatures linked to liver dysfunction and fibrogenesis (2025) · cites this paper as [31]
The Results section, “Hepatic CD8 T cells correlate with NASH in human liver” (page unavailable), reports increased hepatic CD8 T cells in NASH and links their numbers to lobular inflammation and ballooning. It does not identify those cells as CD8+ TEM cells with an exhausted signature or report a fibrosis-related enrichment. The paper also does not report an increase in peripheral-blood CD8+ TEMRA frequency with CAP-assessed steatosis. (LLM, conf=0.84)
Experimental — accuracy not yet measured
During MASH progression, the accumulation of auto-aggressive CD8+ T cells significantly contributes to liver injury and inflammation.
“During the progression of metabolic dysfunction-associated steatohepatitis (MASH), the accumulation of auto-aggressive CD8+ T cells significantly contributes to liver injury and inflammation.”
From SGLT2 inhibitor promotes ketogenesis to improve MASH by suppressing CD8+ T cell activation (2024) · cites this paper as [8]
The Results section, “Hepatic CD8 T cells correlate with NASH in human liver” (page not provided), reports increased hepatic CD8 T cells and significant correlations with lobular inflammation and hepatocyte ballooning. It does not establish that these cells are auto-aggressive or that they cause liver injury and inflammation; the Discussion describes the human findings as associations. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThese T cell functional changes were mirrored by decreased frequencies of XCR1+ cDC1s and increased frequencies of cDC2s.
“These T cell functional changes were mirrored by decreased frequencies of XCR1+ cDC1s (which prime CD8+ T cells) and increased frequencies of cDC2s (which prime CD4+ T cells)”
The NASH T cell response is characterized by an enrichment for cytotoxic CD8+ T, TH1 differentiated CD4+ T and NKT cell populations.
“The NASH T cell response is characterized by an enrichment for cytotoxic CD8+ T, TH1 differentiated CD4+ T and NKT cell populations (18, 121, 131–135).”
From Hepatic Stellate Cell-Immune Interactions in NASH (2022) · cites this paper as [135]
The mechanisms of disease regression are not well understood, but several molecular and cellular principles have been identified from mouse models and from NASH patient samples after regression.
“The mechanisms underlying disease regression are less well understood, but several molecular and cellular principles have been identified based on mouse models24 as well as samples from patients with NASH following disease regression, for example after bariatric surgery or lifestyle modifications.137”
From An integrated view of anti-inflammatory and antifibrotic targets for the treatment of NASH (2023) · cites this paper as [137]
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- Authors
- Haas, J. T., Vonghia, L., Mogilenko, D. A., Verrijken, A., Molendi-Coste, O., Fleury, S., Deprince, A., Nikitin, A., Woitrain, E., Ducrocq-Geoffroy, L., Pic, S., Derudas, B., Dehondt, H., Gheeraert, C., Van Gaal, L., Driessen, A., Lefebvre, P., Staels, B., Francque, S., & Dombrowicz, D.
- Affiliations
- Inserm (FR)
- University of Antwerp (BE)
- Corresponding author
- Vonghia, Luisa
- Dombrowicz, David
- ORCID
- Venue
- Nature Metabolism
- Published
- 2019-06-14
- Volume
- 1
- Issue
- 6
- Pages
- 604-614
- ISSN
- 2522-5812 (ISSN-L)
- PMC
- PMC6837876
- OpenAlex
- W2951755083
- Cited by
- 155
- References
- 55
- Citations by year
- 2026: 14 · 2025: 14 · 2024: 22 · 2023: 31 · 2022: 29 · 2021: 30 · 2020: 14 · 2019: 1
- FWCI
- 14.02
- Type
- journal article
- Language
- en
- Update notices
- correction (2019-06-24)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion, other-oa)
- LillOA (Université de Lille (University Of Lille)) (submittedVersion, other-oa)
- Funders
- Agence Nationale de la Recherche (ANR-18-CE15-0024, ANR-16-RHUS-0006)
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Keywords
- nonalcoholic steatohepatitis, non-alcoholic fatty liver disease, lifestyle intervention, CD8+ T cells, myeloid dendritic cells, antigen presentation, liver inflammation, lobular inflammation, ballooning, diet-induced NASH, hepatocyte injury
- MeSH terms
- Animals, Humans, Liver, Mice, Inbred C57BL, Transcription, Genetic, Mice, Gene Regulatory Networks, Diet, High-Fat, Non-alcoholic Fatty Liver Disease
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