Dectin-1 signaling on colonic γδ T cells promotes psychosocial stress responses
Open accessAbstract
The intestinal immune system interacts with commensal microbiota to maintain gut homeostasis. Furthermore, stress alters the microbiome composition, leading to impaired brain function; yet how the intestinal immune system mediates these effects remains elusive. Here we report that colonic γδ T cells modulate behavioral vulnerability to chronic social stress via dectin-1 signaling. We show that reduction in specific Lactobacillus species, which are involved in T cell differentiation to protect the host immune system, contributes to stress-induced social-avoidance behavior, consistent with our observations in patients with depression. Stress-susceptible behaviors derive from increased differentiation in colonic interleukin (IL)-17-producing γδ T cells (γδ17 T cells) and their meningeal accumulation. These stress-susceptible cellular and behavioral phenotypes are causally mediated by dectin-1, an innate immune receptor expressed in γδ T cells. Our results highlight the previously unrecognized role of intestinal γδ17 T cells in the modulation of psychological stress responses and the importance of dectin-1 as a potential therapeutic target for the treatment of stress-induced behaviors.
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Chronic stress impairs healthy gastrointestinal function, manifesting as dysregulated intestinal motility, microbiota dysbiosis, and low-grade inflammation.
“Growing evidence suggests that chronic stress impairs healthy gastrointestinal function, presenting as dysregulated intestinal motility, dysbiosis of the microbiota and initiation of low-grade inflammation94,95.”
From Central regulation of stress-evoked peripheral immune responses (2023) · cites this paper as [95]
The Results sections on altered microbial communities and colonic T cells report gut-microbiota changes and increased colonic γδ17 T cells in stress-susceptible mice. Our copy does not establish dysregulated intestinal motility or the initiation of low-grade gastrointestinal inflammation, so it supports only part of the cited sentence. (LLM, conf=0.87)
Experimental — accuracy not yet measuredCSDS in mice promotes differentiation of IL17-expressing γδ T cells in the colon via dectin-1 signaling, and neutralizing these cells or knocking out dectin-1 protects against CSDS-induced social avoidance.
“One recent study showed that CSDS in mice promotes differentiation of IL17-expressing γδ T cells in the colon, in a process that is dependent on dectin-1 signaling95. When these cells were neutralized or dectin-1 was genetically knocked out, mice were protected against CSDS-induced social avoidance95.”
From Central regulation of stress-evoked peripheral immune responses (2023) · cites this paper as [95]
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Central regulation of stress-evoked peripheral immune responses
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- Authors
- Zhu, X., Sakamoto, S., Ishii, C., Smith, M. D., Ito, K., Obayashi, M., Unger, L., Hasegawa, Y., Kurokawa, S., Kishimoto, T., Li, H., Hatano, S., Wang, T.-H., Yoshikai, Y., Kano, S.-I., Fukuda, S., Sanada, K., Calabresi, P. A., & Kamiya, A.
- Affiliations
- Johns Hopkins University (US)
- Institute for Advanced Biosciences, Keio University (JP)
- Keio University (JP)
- Southern Illinois University Carbondale (US)
- Medical Institute of Bioregulation, Kyushu University (JP)
- University of Alabama at Birmingham (US)
- University of Tsukuba (JP)
- SHOWA Medical University (JP)
- Corresponding author
- Kamiya, Atsushi
- ORCID
- Venue
- Nature Immunology
- Published
- 2023-03-20
- Volume
- 24
- Issue
- 4
- Pages
- 625-636
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- PMC
- PMC10704545
- OpenAlex
- W4328049092
- Cited by
- 99
- References
- 71
- Citations by year
- 2026: 28 · 2025: 28 · 2024: 24 · 2023: 19
- FWCI
- 9.17
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Johns Hopkins University
- Japan Agency for Medical Research and Development (CREST, JP22gm1010009)
- Japan Dairy Association
- Nestec
- Japan Society for the Promotion of Science (23K24798, CREST, 22H03541)
- National Institute on Aging (R01AG065168)
- National Institute of Mental Health (R21MH128765, R01MH113645, P50MH094268)
- National Institute on Drug Abuse (R01DA041208)
- National Institute of Neurological Disorders and Stroke (R37NS041435, R01NS041435)
- National Center for Complementary and Integrative Health (K01AT010984, R21AT008547)
- Core Research for Evolutional Science and Technology
- Exploratory Research for Advanced Technology (JPMJER1902)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Keywords
- Dectin-1, γδ T cells, psychosocial stress, chronic social stress, depression, Lactobacillus, gut microbiota, IL-17, innate immune receptors, stress-induced behavior
- MeSH terms
- Dectin-1, Colon, Intestines, Signal Transduction, Receptors, Antigen, T-Cell, gamma-delta, Lectins, C-Type
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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