γδ T cells and adipocyte IL-17RC control fat innervation and thermogenesis
Open accessAbstract
The sympathetic nervous system innervates peripheral organs to regulate their function and maintain homeostasis, whereas target cells also produce neurotrophic factors to promote sympathetic innervation 1,2. The molecular basis of this bi-directional communication remains to be fully determined. Here we use thermogenic adipose tissue from mice as a model system to show that T cells, specifically γδ T cells, have a crucial role in promoting sympathetic innervation, at least in part by driving the expression of TGFβ1 in parenchymal cells via the IL-17 receptor C (IL-17RC). Ablation of IL-17RC specifically in adipose tissue reduces expression of TGFβ1 in adipocytes, impairs local sympathetic innervation and causes obesity and other metabolic phenotypes that are consistent with defective thermogenesis; innervation can be fully rescued by restoring TGFβ1 expression. Ablating γδ Τ cells and the IL-17RC signalling pathway also impairs sympathetic innervation in other tissues such as salivary glands. These findings demonstrate coordination between T cells and parenchymal cells to regulate sympathetic innervation.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Loss of IL-17Ra in the somatosensory cortex (S1DZ) has previously been implicated in neuronal IL-17a signaling to mediate social abnormalities.
“Loss of IL-17Ra in the somatosensory cortex (S1DZ), previously implicated in neuronal IL-17a signaling to mediate social abnormalities1,23, also decreased anxiety levels of animals (Extended Data Fig. 5k)”
From Meningeal γδ T cells regulate anxiety-like behavior via IL-17a signaling in neurons (2020) · cites this paper as [23]
IL-17a regulates social behavior in maternal immune activation models.
“Previously described non-immune properties of IL-17 included (i) the regulation of social behavior in MIA models1,23”
From Meningeal γδ T cells regulate anxiety-like behavior via IL-17a signaling in neurons (2020) · cites this paper as [23]
Embryonic IL-17Ra signaling on S1DZ results in social impairment, while the same signaling during adulthood promotes sociability.
“While embryonic IL-17Ra signaling on S1DZ results in social impairment1, same signaling during adulthood promotes sociability23.”
From Meningeal γδ T cells regulate anxiety-like behavior via IL-17a signaling in neurons (2020) · cites this paper as [23]
IL-17Ra has been observed in cortical neurons in a mouse model of maternal immune activation.
“IL-17a receptor subunit a (IL-17Ra) has been observed in cortical neurons in a mouse model of maternal immune activation (MIA)23.”
From Meningeal γδ T cells regulate anxiety-like behavior via IL-17a signaling in neurons (2020) · cites this paper as [23]
The behavioral phenotype observed in the absence of neuronal IL-17Ra is complex and is not limited to the prefrontal cortex.
“Loss of IL-17Ra in the somatosensory cortex (S1DZ), previously implicated in neuronal IL-17a signaling to mediate social abnormalities1,23, also decreased anxiety levels of animals (Extended Data Fig. 5k), indicating that the behavioral phenotype observed in the absence of neuronal IL-17Ra is complex and is not limited to prefrontal cortex.”
From Meningeal γδ T cells regulate anxiety-like behavior via IL-17a signaling in neurons (2020) · cites this paper as [23]
Loss of IL-17Ra in the somatosensory cortex (S1DZ) also decreases anxiety levels of animals.
“Loss of IL-17Ra in the somatosensory cortex (S1DZ), previously implicated in neuronal IL-17a signaling to mediate social abnormalities1,23, also decreased anxiety levels of animals (Extended Data Fig. 5k), indicating that the behavioral phenotype observed in the absence of neuronal IL-17Ra is complex and is not limited to prefrontal cortex.”
From Meningeal γδ T cells regulate anxiety-like behavior via IL-17a signaling in neurons (2020) · cites this paper as [23]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 48 · Cited by 180
Research works printed but not linked: 1
- [33]Cheng L Identification of spinal circuits involved in touch-evoked dynamic mechanical pain. Nat Neurosci 20, 804– 814, doi: 10.1038/nn.4549 (2017). 28436981 PMC5470641 · DOI · Paper page
- Authors
- Hu, B., Jin, C., Zeng, X., Resch, J. M., Jedrychowski, M. P., Yang, Z., Desai, B. N., Banks, A. S., Lowell, B. B., Mathis, D., & Spiegelman, B. M.
- Affiliations
- Harvard University (US)
- Koch Institute for Integrative Cancer Research At MIT (US)
- Beth Israel Deaconess Medical Center (US)
- Corresponding author
- Spiegelman, Bruce M.
- ORCID
- Venue
- Nature
- Published
- 2020-02-19
- Volume
- 578
- Issue
- 7796
- Pages
- 610-614
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC7055484
- OpenAlex
- W3008967181
- Cited by
- 180
- References
- 48
- Citations by year
- 2026: 18 · 2025: 23 · 2024: 26 · 2023: 37 · 2022: 35 · 2021: 24 · 2020: 17
- FWCI
- 17.00
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Cancer Institute (K99CA226400, R00CA226400)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK031405, R37DK031405, R01DK092541)
- National Institute of Neurological Disorders and Stroke (P30NS072030)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- γδ T cells, IL-17RC, adipocytes, sympathetic innervation, thermogenesis, thermogenic adipose tissue, TGF-β1, obesity, cold tolerance, salivary glands, neuroimmune interactions
- MeSH terms
- Parenchymal Tissue, Adipose Tissue, Animals, Adipose Tissue, Brown, Male, Organ Specificity, Sympathetic Nervous System, T-Lymphocytes, Signal Transduction, Adipocytes, Mice, Knockout, Interleukin-17, Thermogenesis, Mice, Transforming Growth Factor beta1
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 ›
Are you an author, or do you see a problem with this page? Request a review
