How and why do T cells and their derived cytokines affect the injured and healthy brain?
Open accessAbstract
The evolution of adaptive immunity provides enhanced defence against specific pathogens, as well as homeostatic immune surveillance of all tissues. Despite being 'immune privileged', the CNS uses the assistance of the immune system in physiological and pathological states. In this Opinion article, we discuss the influence of adaptive immunity on recovery after CNS injury and on cognitive and social brain function. We further extend a hypothesis that the pro-social effects of interferon-regulated genes were initially exploited by pathogens to increase host-host transmission, and that these genes were later recycled by the host to form part of an immune defence programme. In this way, the evolution of adaptive immunity may reflect a host-pathogen 'arms race'.
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CD4+ cells modulate mood and learning and memory.
“CD4+ cells modulate mood and learning and memory, actions that mainly have been demonstrated using lymphopenic mice, such as T cell- and B cell-deficient Rag2−/− mice, that were replenished with adoptive transfer of splenocytes or lymphoid cells (Brachman et al., 2015; Clark et al., 2016; Filiano et al., 2017).”
From Distinct characteristics of hippocampal pathogenic th17 cells in a mouse model of depression (2018) · cites this paper as Filiano et al., 2017
CXCR6 is significantly enriched on meningeal γδ17 T cells compared to spleen.
“Analysis of chemokine receptor expression in each γδ T cell population revealed a significant enrichment of CXCR6 (a chemokine receptor highly expressed in activated/memory T cells11) on meningeal γδ17 T cells when compared to the spleen (Fig. 2e).”
From Meningeal γδ T cells regulate anxiety-like behavior via IL-17a signaling in neurons (2020) · cites this paper as [11]
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Self-citation
- Authors
- Filiano, A. J., Gadani, S. P., & Kipnis, J.
- Affiliations
- University of Virginia (US)
- Corresponding author
- Filiano, Anthony J.
- Kipnis, Jonathan
- Venue
- Nature Reviews Neuroscience
- Published
- 2017-04-27
- Volume
- 18
- Issue
- 6
- Pages
- 375-384
- ISSN
- 1471-003X (ISSN-L)
- 1471-0048
- PMC
- PMC5823005
- OpenAlex
- W2607931113
- Cited by
- 199
- References
- 127
- Citations by year
- 2026: 7 · 2025: 4 · 2024: 38 · 2023: 22 · 2022: 22 · 2021: 31 · 2020: 22 · 2019: 21 · 2018: 25 · 2017: 7
- FWCI
- 1.98
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature reviews. Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG034113, R37AG034113)
- National Institute of Mental Health (R21MH108156, R33MH108156)
- National Institute of General Medical Sciences (T32GM007267)
- National Institute of Allergy and Infectious Diseases (T32AI007496)
- National Institute of Neurological Disorders and Stroke (R01NS096967)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- T cells, cytokines, interferon-gamma, adaptive immunity, immune privilege, immune surveillance, host-pathogen arms race, interferon-regulated genes, social behavior, cognitive function, neuroinflammation
- MeSH terms
- Brain Injuries, Traumatic, Animals, Brain, Brain Injuries, Humans, T-Lymphocytes, Cytokines, Adaptive Immunity
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