Tet2 deficiency drives liver microbiome dysbiosis triggering Tc1 cell autoimmune hepatitis
Open accessAbstract
The triggers that drive interferon-γ (IFNγ)-producing CD8 T cell (Tc1 cell)-mediated autoimmune hepatitis (AIH) remain obscure. Here, we show that lack of hematopoietic Tet methylcytosine dioxygenase 2 (Tet2), an epigenetic regulator associated with autoimmunity, results in the development of microbiota-dependent AIH-like pathology, accompanied by hepatic enrichment of aryl hydrocarbon receptor (AhR) ligand-producing pathobionts and rampant Tc1 cell immunity. We report that AIH-like disease development is dependent on both IFNγ and AhR signaling, as blocking either reverts ongoing AIH-like pathology. Illustrating the critical role of AhR-ligand-producing pathobionts in this condition, hepatic translocation of the AhR ligand indole-3-aldehyde (I3A)-releasing Lactobacillus reuteri is sufficient to trigger AIH-like pathology. Finally, we demonstrate that I3A is required for L. reuteri-induced Tc1 cell differentiation in vitro and AIH-like pathology in vivo, both of which are restrained by Tet2 within CD8 T cells. This AIH-disease model may contribute to the development of therapeutics to alleviate AIH.
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Prior work showed that the microbial AhR agonist indole-3-aldehyde enhances Tc1 immunity, aggravates autoimmunity, and improves ICI efficacy.
“Prior work demonstrated that the microbial AhR agonist indole-3-aldehyde enhances Tc1 immunity, aggravating autoimmunity46 and improving ICI efficacy32,47.”
From Exercise-induced microbiota metabolite enhances CD8 T cell antitumor immunity promoting immunotherapy efficacy (2025) · cites this paper as [46]
In earlier work, CD8 T cells lacking Tet2 were more responsive to I3A and exogenous IFNγ.
“we recently showed the absence of the epigenetic regulator Tet2 within CD8 T cells renders them more sensitive to I3A and exogenous IFNγ29”
From Dietary tryptophan metabolite released by intratumoral Lactobacillus reuteri facilitates immune checkpoint inhibitor treatment (2023) · cites this paper as [29]
Lr and elevated dietary Trp worsen autoimmune responses in preclinical models.
“We29 and others31,34 uncovered that Lr and elevated dietary Trp aggravates autoimmune responses in preclinical models.”
From Dietary tryptophan metabolite released by intratumoral Lactobacillus reuteri facilitates immune checkpoint inhibitor treatment (2023) · cites this paper as [29]
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- Authors
- Pandey, S. P., Bender, M. J., McPherson, A. C., Phelps, C. M., Sanchez, L. M., Rana, M., Hedden, L., Sangani, K. A., Chen, L., Shapira, J. H., Siller, M., Goel, C., Verdú, E. F., Jabri, B., Chang, A., Chandran, U. R., Mullett, S. J., Wendell, S. G., Singhi, A. D., Tilstra, J. S., Pierre, J. F., Arteel, G. E., Hinterleitner, R., & Meisel, M.
- Affiliations
- University of Pittsburgh (US)
- University of Chicago (US)
- University of Wisconsin–Madison (US)
- Corresponding author
- Meisel, Marlies
- ORCID
- Venue
- Cell Host & Microbe
- Publisher
- Elsevier BV
- Published
- 2022-07
- Volume
- 30
- Issue
- 7
- Pages
- 1003-1019.e10
- ISSN
- 1931-3128 (ISSN-L)
- PMC
- PMC9841318
- OpenAlex
- W4281652082
- Cited by
- 72
- References
- 97
- Citations by year
- 2026: 16 · 2025: 24 · 2024: 12 · 2023: 14 · 2022: 6
- FWCI
- 8.34
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 377 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell Host & Microbe (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (1s10od023402-01a1)
- National Institute on Alcohol Abuse and Alcoholism (R01AA021978)
- National Cancer Institute (R21CA259636, R01CA253329, P30CA047904)
- National Institute of General Medical Sciences (T32GM007281)
- National Institute of Allergy and Infectious Diseases (R21AI163721, R21AI163503, T32AI089443)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK120531, R01DK130897)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (K08AR075056)
- Topics
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- TET2, autoimmune hepatitis, dysbiosis, Tc1 cells, CD8+ T cells, aryl hydrocarbon receptor, indole-3-carboxaldehyde, Lactobacillus reuteri, pathobionts, interferon-gamma, epigenetic regulation, gut-liver axis, autoimmunity
- MeSH terms
- Animals, DNA-Binding Proteins, Interferon-gamma, Ligands, Liver, T-Lymphocytes, Cytotoxic, Hepatitis, Autoimmune, Dioxygenases, Mice, Limosilactobacillus reuteri, Microbiota, Dysbiosis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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