T cell receptor/CARMA1/NF-κB signaling controls T-helper (Th) 17 differentiation
Open accessAbstract
IL-17-producing CD4 T cells play a key role in immune responses against extracellular bacteria and autoimmunity. Nuclear factor κB (NF-κB) is required for T-cell activation and selected effector functions, but its role in Th17 differentiation is controversial. Using genetic mouse models that impede T-cell-NF-κB signaling either downstream of the T-cell receptor (TCR) or of IκB kinase β (IKKβ), we demonstrate that NF-κB signaling controls not only survival and proliferation of activated T cells, but, if cell survival and cell-cycle progression are enabled, has an additional role in promoting completion of Th17 differentiation. CARD-containing MAGUK protein 1 (CARMA1), an adapter required for TCR/NF-κB signaling, was necessary for acquisition of IL-17A, IL-17F, IL-21, IL-22, IL-23R, and CCR6 expression in T cells cultured under Th17 conditions. In proliferating cells, lack of CARMA1 selectively prevented Th17, but not Th1 or Th2 differentiation, in a cell-intrinsic manner. Consistent with these data, CARMA1-KO mice were resistant to experimental autoimmune encephalomyelitis. Surprisingly, transcription factors essential for Th17 differentiation such as RORγt, AHR, and IRF4 were normally induced in CARMA1-KO T cells activated under Th17 conditions, suggesting that the Th17 differentiation program was initiated normally. Instead, chromatin loci of Th17 effector molecules failed to acquire an open conformation in CARMA1-KO T cells. Our results demonstrate that TCR/CARMA1/NF-κB controls completion of Th17 differentiation by enabling chromatin accessibility of Th17 effector molecule loci.
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Mutations in downstream molecules involved in SYK signaling, including BCL10 and MALT1, have also been associated with MS risk.
“Likewise, mutations in downstream molecules involved in SYK signaling, including BCL10 and MALT1, have also been associated with MS risk (Mc Guire et al., 2013; Molinero et al., 2012).”
From SYK coordinates neuroprotective microglial responses in neurodegenerative disease (2022) · cites this paper as Molinero et al., 2012
The Results identify Bcl10 and MALT1 as members of a T-cell signaling complex, and the Discussion mentions multiple sclerosis as a disease with a strong Th17 component. Neither passage reports that mutations in BCL10 or MALT1 are associated with MS risk, and the signaling described is T-cell receptor/CARMA1 signaling rather than SYK signaling. No page numbers were provided for these passages. (LLM, conf=0.84)
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Marraffa, A. P., Berrevoets, C., Mosiello, M., Wijers, R., Roelofs, D., van Brakel, M., Kroese, K., Peeters, M. J. W., Dik, W. A., Kunert, A., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.10.14.682056
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Natural flavonoids in multiple sclerosis: molecular insights and emerging therapeutic strategies
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T cell receptors equipped with ICOS provide T cells with durable anti-tumor response
Marraffa, A. P., Berrevoets, C., Mosiello, M., Coelho, R. M. L., Roelofs, D., van Brakel, M., Wijers, R., Kroese, K., Peeters, M. J. W., Dik, W. A., et al. (2026) · Molecular Cancer · doi:10.1186/s12943-026-02765-9
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Genetic and immunological characterization of a hyper-IgE Syndrome pedigree
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- Authors
- Molinero, L. L., Cubre, A., Mora-Solano, C., Wang, Y., & Alegre, M.-L.
- Affiliations
- University of Chicago (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2012-10-03
- Volume
- 109
- Issue
- 45
- Pages
- 18529-18534
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC3494911
- OpenAlex
- W2042298055
- Cited by
- 61
- References
- 35
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 3 · 2023: 2 · 2022: 3 · 2021: 6 · 2020: 1 · 2019: 3 · 2018: 6 · 2017: 5 · 2016: 4 · 2015: 9 · 2014: 8 · 2013: 3
- FWCI
- 2.80
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (R01AI052352, R01 AI1052352)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- Th17 cell differentiation, CARMA1, NF-κB signaling, T cell receptor signaling, IκB kinase β, IL-17, chromatin accessibility, experimental autoimmune encephalomyelitis, autoimmunity, RORγt, IRF4, AHR, CD4+ T cells
- MeSH terms
- Animals, Cell Differentiation, Chromatin, Female, Mice, Inbred C57BL, Receptors, Antigen, T-Cell, Transcription Factors, Signal Transduction, NF-kappa B, Mice, Knockout, Cross-Priming, Mitogen-Activated Protein Kinase 9, STAT3 Transcription Factor, STAT5 Transcription Factor, Mice, CARD Signaling Adaptor Proteins, Genetic Loci, Th17 Cells
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