NAD+ protects against EAE by regulating CD4+ T-cell differentiation
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CD4+ T cells are involved in the development of autoimmunity, including multiple sclerosis (MS). Here we show that nicotinamide adenine dinucleotide (NAD+) blocks experimental autoimmune encephalomyelitis (EAE), a mouse model of MS, by inducing immune homeostasis through CD4+IFNγ+IL-10+ T cells and reverses disease progression by restoring tissue integrity via remyelination and neuroregeneration. We show that NAD+ regulates CD4+ T-cell differentiation through tryptophan hydroxylase-1 (Tph1), independently of well-established transcription factors. In the presence of NAD+, the frequency of T-bet−/− CD4+IFNγ+ T cells was twofold higher than wild-type CD4+ T cells cultured in conventional T helper 1 polarizing conditions. Our findings unravel a new pathway orchestrating CD4+ T-cell differentiation and demonstrate that NAD+ may serve as a powerful therapeutic agent for the treatment of autoimmune and other diseases. The mechanism by which NAD+ alters the systemic immune response is unclear. Here the authors show that NAD+ induces systemic homeostasis and protects against experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis, by regulating CD4+T cell differentiation and promoting myelin and axonal regeneration.
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NAD+ seems to exhibit immunomodulatory properties, such as influencing T cell polarization.
“NAD+ seems to exhibit immunomodulatory properties, such as influencing T cell polarization112,113”
From NAD+ metabolism and its roles in cellular processes during ageing (2021) · cites this paper as [112]
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Self-citation
- Authors
- Tullius, S. G., Biefer, H. R. C., Li, S., Trachtenberg, A. J., Edtinger, K., Quante, M., Krenzien, F., Uehara, H., Yang, X., Kissick, H. T., Kuo, W. P., Ghiran, I., de la Fuente, M. A., Arredouani, M. S., Camacho, V., Tigges, J. C., Toxavidis, V., El Fatimy, R., Smith, B. D., Vasudevan, A., & ElKhal, A.
- Affiliations
- Brigham and Women's Hospital (US)
- Harvard University (US)
- Beth Israel Deaconess Medical Center (US)
- Corresponding author
- ElKhal, Abdallah
- ORCID
- Venue
- Nature Communications
- Published
- 2014-10-07
- Volume
- 5
- Issue
- 1
- Pages
- 5101-5101
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4205890
- OpenAlex
- W2097813112
- Cited by
- 107
- References
- 64
- Citations by year
- 2026: 4 · 2025: 10 · 2024: 10 · 2023: 14 · 2022: 16 · 2021: 11 · 2020: 13 · 2019: 5 · 2018: 6 · 2017: 9 · 2016: 5 · 2015: 4
- FWCI
- 2.74
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Nature Communications (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- UVaDOC UVaDOC University of Valladolid Documentary Repository (University of Valladolid) (submittedVersion, other-oa)
- RePEc: Research Papers in Economics (submittedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by-nc-nd)
- Hispana (submittedVersion, cc-by-nc-nd)
- University of Valladolid Documentary Repository (University of Valladolid) (submittedVersion, cc-by-nc-nd)
- Funders
- National Institute on Aging (R01AG039449)
- National Heart, Lung, and Blood Institute (R01HL096795)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- NAD+, experimental autoimmune encephalomyelitis, multiple sclerosis, CD4+ T cell differentiation, tryptophan hydroxylase 1, T-bet, immune homeostasis, remyelination, nerve regeneration, axon regeneration, autoimmunity
- MeSH terms
- Animals, Cell Differentiation, Disease Models, Animal, Encephalomyelitis, Autoimmune, Experimental, Homeostasis, Multiple Sclerosis, Myelin Sheath, NAD, Regeneration, Tryptophan Hydroxylase, CD4-Positive T-Lymphocytes, Mice
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