Featured
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Brain control of humoral immune responses amenable to behavioural modulation
Neuronal activities in the central amygdala and paraventricular nucleus are transmitted via the splenic nerve to increase plasma cell formation after immunization, and this process can be behaviourally enhanced in mice.
- Xu Zhang
- , Bo Lei
- & Hai Qi
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Article |
AIM2 inflammasome surveillance of DNA damage shapes neurodevelopment
The sensing of DNA damage by the AIM2 inflammasome promotes the death of central nervous system cells and is required for normal brain development.
- Catherine R. Lammert
- , Elizabeth L. Frost
- & John R. Lukens
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Article |
γδ T cells and adipocyte IL-17RC control fat innervation and thermogenesis
Vγ6+ Vδ1+ γδ T cells control tolerance to cold by activating adipocyte IL-17RC and promoting sympathetic innervation of thermogenic adipose tissue in mice.
- Bo Hu
- , Chengcheng Jin
- & Bruce M. Spiegelman
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Article |
Feeding-dependent VIP neuron–ILC3 circuit regulates the intestinal barrier
Feeding controls a neuroimmune circuit comprising VIP-producing neurons and type-3 innate lymphoid cells that helps to regulate the efficiency of nutrient uptake and IL-22-mediated immune protection in the intestine.
- Jhimmy Talbot
- , Paul Hahn
- & Dan R. Littman
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VEGF-C-driven lymphatic drainage enables immunosurveillance of brain tumours
In a mouse model of glioblastoma, treatment with VEGF-C increases lymphatic drainage in the central nervous system and improves the immune response, suggesting that modulating meningeal lymphatics could enhance checkpoint inhibitor therapy.
- Eric Song
- , Tianyang Mao
- & Akiko Iwasaki
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Clonally expanded CD8 T cells patrol the cerebrospinal fluid in Alzheimer’s disease
An integrated analysis of several cohorts shows that clonal, antigen-experienced T cells are found in the cerebrospinal fluid of patients with Alzheimer’s disease, suggesting that the adaptive immune system has a role in age-related neurodegeneration.
- David Gate
- , Naresha Saligrama
- & Tony Wyss-Coray
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IL-17a promotes sociability in mouse models of neurodevelopmental disorders
IL-17a induced by immune activation affects cortical neural activity and promotes social interaction in a mouse model of neurodevelopmental disorders.
- Michael Douglas Reed
- , Yeong Shin Yim
- & Gloria B. Choi
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Article |
The microbiota regulate neuronal function and fear extinction learning
A diverse intestinal microbiota is required for mice to undergo extinction-related neuronal plasticity and normal fear extinction learning.
- Coco Chu
- , Mitchell H. Murdock
- & David Artis
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Article |
Neuronal vulnerability and multilineage diversity in multiple sclerosis
Single-cell RNA sequencing was used to construct a map of gene expression in lesions from brains of patients with multiple sclerosis, revealing distinct lineage- and region-specific transcriptomic changes associated with selective cortical neuron damage and glial activation.
- Lucas Schirmer
- , Dmitry Velmeshev
- & David H. Rowitch
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Single-cell analysis reveals T cell infiltration in old neurogenic niches
Single-cell transcriptomic analysis of neurogenic niches in young and old mice reveals that T cells infiltrate the neurogenic niches of old mice and inhibit the proliferation of neural stem cells, in part through expression of interferon-γ.
- Ben W. Dulken
- , Matthew T. Buckley
- & Anne Brunet
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β-Synuclein-reactive T cells induce autoimmune CNS grey matter degeneration
In a rat model of multiple sclerosis, β-synuclein-specific T cells induce inflammation and pathological changes in the grey matter of the central nervous system; these cells were also found in higher numbers in patients with multiple sclerosis, particularly those with a chronic progressive course.
- Dmitri Lodygin
- , Moritz Hermann
- & Alexander Flügel
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Letter |
Spatial and temporal heterogeneity of mouse and human microglia at single-cell resolution
Analyses at single-cell resolution show that diverse subtypes of microglia exist during development and homeostasis of the central nervous system, and identify specific subsets of microglia associated with demyelination and neurodegenerative disease in mice and humans.
- Takahiro Masuda
- , Roman Sankowski
- & Marco Prinz
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Letter |
Brain regulatory T cells suppress astrogliosis and potentiate neurological recovery
In a mouse model of ischaemic stroke, regulatory T cells infiltrate the injured brain in response to the chemokines CCL1 and CCL20 and suppress excessive astrogliosis via the production of amphiregulin.
- Minako Ito
- , Kyoko Komai
- & Akihiko Yoshimura
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Article |
T cells in patients with narcolepsy target self-antigens of hypocretin neurons
The detection of hypocretin-specific autoreactive CD4+ and CD8+ T cells in patients with narcolepsy reveals the autoimmune aetiology of this disorder.
- Daniela Latorre
- , Ulf Kallweit
- & Federica Sallusto
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Article |
Functional aspects of meningeal lymphatics in ageing and Alzheimer’s disease
Meningeal lymphatic dysfunction promotes amyloid-β deposition in the meninges and worsens brain amyloid-β pathology, acting as an aggravating factor in Alzheimer’s disease and in age-associated cognitive decline; improving meningeal lymphatic function could help to prevent or delay age-associated neurological diseases.
- Sandro Da Mesquita
- , Antoine Louveau
- & Jonathan Kipnis
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Letter |
Microglial control of astrocytes in response to microbial metabolites
TGFα and VEGF-B produced by microglia regulate astrocyte function in the experimental autoimmune encephalomyelitis model of multiple sclerosis.
- Veit Rothhammer
- , Davis M. Borucki
- & Francisco J. Quintana
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Article |
Innate immune memory in the brain shapes neurological disease hallmarks
Peripheral stimuli can induce acute immune training and tolerance in the brain and lead to long-lasting epigenetic reprogramming of microglia; these changes alter pathology in mouse models of stroke and Alzheimer’s pathology .
- Ann-Christin Wendeln
- , Karoline Degenhardt
- & Jonas J. Neher
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Reversing behavioural abnormalities in mice exposed to maternal inflammation
The authors define a specific cortical subregion of the somatosensory cortex as a critical region of dysfunction that is causal to the emergence of abnormal social and repetitive behaviours in mice exposed to maternal inflammation.
- Yeong Shin Yim
- , Ashley Park
- & Gloria B. Choi
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Letter |
Maternal gut bacteria promote neurodevelopmental abnormalities in mouse offspring
Maternal immune activation (MIA)-mediated abnormal behavioural phenotypes require defined gut commensal bacteria for the induction of IL-17-producing T helper 17 cells.
- Sangdoo Kim
- , Hyunju Kim
- & Jun R. Huh
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Letter |
The neuropeptide neuromedin U stimulates innate lymphoid cells and type 2 inflammation
Intestinal type 2 innate lymphoid cells express the neuropeptide receptor NMUR1, which makes them responsive to neuronal neuromedin U, thereby promoting a type 2 cytokine response and accelerated expulsion of the gastro-intestinal nematode Nippostrongylus brasiliensis.
- Christoph S. N. Klose
- , Tanel Mahlakõiv
- & David Artis
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Letter |
A somatic mutation in erythro-myeloid progenitors causes neurodegenerative disease
Braf V600E expression in resident macrophage progenitors leads to clonal expansion of ERK-activated microglia, which causes synaptic and neuronal loss in the brain and results in lethal neurodegenerative disease in adult mice.
- Elvira Mass
- , Christian E. Jacome-Galarza
- & Frederic Geissmann
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Letter |
T cells from patients with Parkinson’s disease recognize α-synuclein peptides
Epitopes derived from two regions of α-synuclein elicit immune responses in patients with Parkinson’s disease, involving IL-5-secreting CD4+ T cells, as well as IFNγ-secreting CD8+ cytotoxic T cells.
- David Sulzer
- , Roy N. Alcalay
- & Alessandro Sette
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Letter |
Microglia-dependent synapse loss in type I interferon-mediated lupus
Abnormal behavioural phenotypes and synapse loss in the brain of lupus-prone mice are prevented by blocking type I interferon signalling, which is further shown to stimulate microglial phagocytosis of neuronal material in the brains of these mice.
- Allison R. Bialas
- , Jessy Presumey
- & Michael C. Carroll
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Letter |
Human umbilical cord plasma proteins revitalize hippocampal function in aged mice
Treatment with plasma of an early developmental stage, human umbilical cord, revitalizes the hippocampus and improves cognitive function in aged mice.
- Joseph M. Castellano
- , Kira I. Mosher
- & Tony Wyss-Coray
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Letter |
Unexpected role of interferon-γ in regulating neuronal connectivity and social behaviour
Adaptive immune dysfunction, in particular interferon-γ, is implicated in disorders characterized by social dysfunction and suggests interferon-γ signalling may provide a co-evolutionary link between social behaviour and an anti-pathogen immune response.
- Anthony J. Filiano
- , Yang Xu
- & Jonathan Kipnis
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Letter |
A complement–microglial axis drives synapse loss during virus-induced memory impairment
People infected with West Nile virus often experience cognitive side effects including memory loss through unknown mechanisms; mice and humans infected with the virus experience a loss in hippocampal presynaptic terminals, which can be reversed by disrupting complement or microglia in mice.
- Michael J. Vasek
- , Charise Garber
- & Robyn S. Klein
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Letter |
Effector T-cell trafficking between the leptomeninges and the cerebrospinal fluid
By investigating trafficking of autoreactive T cells into the CSF during experimental autoimmune encephalitis, the authors find that T cells enter the CSF from the leptomeninges, and that commuting between the leptomeninges and the CSF is regulated by integrin adhesive forces triggered by T-cell activation and/or chemokines.
- Christian Schläger
- , Henrike Körner
- & Alexander Flügel
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Letter |
Structural and functional features of central nervous system lymphatic vessels
The central nervous system undergoes constant immune surveillance, but the route that immune cells take to exit the brain has been unclear as it had been thought to lack a classical lymphatic drainage system; here functional lymphatic vessels able to carry both fluid and immune cells from the cerebrospinal fluid are shown to be located in the brain meninges.
- Antoine Louveau
- , Igor Smirnov
- & Jonathan Kipnis
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Letter |
Human intracellular ISG15 prevents interferon-α/β over-amplification and auto-inflammation
ISG15 deficiency in humans leads to a failure to maintain adequate levels of USP18, triggering an increase in type I interferon production and signalling, and promoting auto-inflammatory disease.
- Xianqin Zhang
- , Dusan Bogunovic
- & Sandra Pellegrini
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Letter |
Nociceptive sensory neurons drive interleukin-23-mediated psoriasiform skin inflammation
In mice, it is possible to induce a psoriasis-like condition by applying imiquimod; here, the production of interleukin-23 that is stimulated by such skin inflammation is shown to depend on the interaction of nociceptors expressing the Nav1.8 and TRPV1 channels with skin-resident dendritic cells.
- Lorena Riol-Blanco
- , Jose Ordovas-Montanes
- & Ulrich H. von Andrian
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Letter |
Transcranial amelioration of inflammation and cell death after brain injury
Using long-term intravital photography to explore the cellular changes after compression-induced traumatic brain injury in a murine model, it is shown that parenchymal and meningeal inflammation as well as cell death can be modulated by topical treatment with purinergic receptor antagonists and glutathione.
- Theodore L. Roth
- , Debasis Nayak
- & Dorian B. McGavern
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Article |
Bacteria activate sensory neurons that modulate pain and inflammation
This study shows that most known mediators of immunity, such as TLR2, MyD88, T cells or B cells, and neutrophils and monocytes, are dispensable for pain produced by Staphylococcus aureus infection; instead, bacterial products, such as N-formylated peptides and α-haemolysin, induce pain by directly activating nociceptor neurons, which in turn modulate inflammation.
- Isaac M. Chiu
- , Balthasar A. Heesters
- & Clifford J. Woolf
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Letter |
Suppression of neuroinflammation by astrocytic dopamine D2 receptors via αB-crystallin
Chronic inflammation is a feature of the ageing brain and some neurodegenerative diseases; the authors show that astrocytes normally suppress neuroinflammation through activation of their DRD2 receptor by CRYAB, potentially opening new avenues for treatments.
- Wei Shao
- , Shu-zhen Zhang
- & Jia-wei Zhou
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Research Highlights |
A boost to the brain's barrier
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Research Highlights |
T cell makes nerve molecule
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Research Highlights |
Neuroimmunology: Immune input for retinal repair
C9orf72 suppresses systemic and neural inflammation induced by gut bacteria