6 results match your criteria Brain Behavior and Immunity [Journal]

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Cell-Type-Specific Interleukin 1 Receptor 1 Signaling in the Brain Regulates Distinct Neuroimmune Activities.

Immunity 2019 Jan 16. Epub 2019 Jan 16.

Institute for Behavioral Medicine Research, College of Medicine, The Ohio State University, Columbus, OH 43210, USA; Division of Biosciences, College of Dentistry, The Ohio State University, Columbus, OH 43210, USA. Electronic address:

Interleukin-1 (IL-1) signaling is important for multiple potentially pathogenic processes in the central nervous system (CNS), but the cell-type-specific roles of IL-1 signaling are unclear. We used a genetic knockin reporter system in mice to track and reciprocally delete or express IL-1 receptor 1 (IL-1R1) in specific cell types, including endothelial cells, ventricular cells, peripheral myeloid cells, microglia, astrocytes, and neurons. We found that endothelial IL-1R1 was necessary and sufficient for mediating sickness behavior and drove leukocyte recruitment to the CNS and impaired neurogenesis, whereas ventricular IL-1R1 was critical for monocyte recruitment to the CNS. Read More

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http://dx.doi.org/10.1016/j.immuni.2018.12.012DOI Listing
January 2019

TREMendous 2 Be Social.

Immunity 2018 05;48(5):842-843

Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; Evergrande Center for Immunologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Electronic address:

TREM2 is known for its role in microglial phagocytosis and in neurodegenerative diseases. In this issue of Immunity, Filipello et al. (2018) show that microglial TREM2 is required for synaptic pruning in early development. Read More

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http://dx.doi.org/10.1016/j.immuni.2018.04.034DOI Listing
May 2018
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The Microglial Innate Immune Receptor TREM2 Is Required for Synapse Elimination and Normal Brain Connectivity.

Immunity 2018 05 8;48(5):979-991.e8. Epub 2018 May 8.

Laboratory of Pharmacology and Brain Pathology, Humanitas Clinical and Research Center, Via Manzoni 56, 20089 Rozzano - Milan, Italy; IN-CNR, 20129 Milano, Italy. Electronic address:

The triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial innate immune receptor associated with a lethal form of early, progressive dementia, Nasu-Hakola disease, and with an increased risk of Alzheimer's disease. Microglial defects in phagocytosis of toxic aggregates or apoptotic membranes were proposed to be at the origin of the pathological processes in the presence of Trem2 inactivating mutations. Here, we show that TREM2 is essential for microglia-mediated synaptic refinement during the early stages of brain development. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S10747613183018
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http://dx.doi.org/10.1016/j.immuni.2018.04.016DOI Listing
May 2018
15 Reads

Brain Endothelial- and Epithelial-Specific Interferon Receptor Chain 1 Drives Virus-Induced Sickness Behavior and Cognitive Impairment.

Immunity 2016 Apr;44(4):901-12

Institute of Neuropathology, University of Freiburg, 79106 Freiburg, Germany; BIOSS Centre for Biological Signalling Studies, University of Freiburg, 79104 Freiburg, Germany. Electronic address:

Sickness behavior and cognitive dysfunction occur frequently by unknown mechanisms in virus-infected individuals with malignancies treated with type I interferons (IFNs) and in patients with autoimmune disorders. We found that during sickness behavior, single-stranded RNA viruses, double-stranded RNA ligands, and IFNs shared pathways involving engagement of melanoma differentiation-associated protein 5 (MDA5), retinoic acid-inducible gene 1 (RIG-I), and mitochondrial antiviral signaling protein (MAVS), and subsequently induced IFN responses specifically in brain endothelia and epithelia of mice. Behavioral alterations were specifically dependent on brain endothelial and epithelial IFN receptor chain 1 (IFNAR). Read More

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http://dx.doi.org/10.1016/j.immuni.2016.04.005DOI Listing
April 2016
53 Reads

Bugs and Brain: How Infection Makes You Feel Blue.

Immunity 2016 Apr;44(4):718-20

Center for Brain Immunology and Glia (BIG), Department of Neuroscience, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA. Electronic address:

In this issue of Immunity, Prinz and colleagues (2016) describe an unexpected mechanism underlying the role of type I interferon in the initiation of cognitive impairment and sickness behavior during viral infection through induction of chemokine CXCL10 in central nervous system epithelial and endothelial cells. Read More

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http://dx.doi.org/10.1016/j.immuni.2016.03.010DOI Listing
April 2016
18 Reads

Behavior of parasite-specific effector CD8+ T cells in the brain and visualization of a kinesis-associated system of reticular fibers.

Immunity 2009 Feb 22;30(2):300-11. Epub 2009 Jan 22.

Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

To understand lymphocyte behavior in the brain, we used two-photon microscopy to visualize effector CD8(+) T cells during toxoplasmic encephalitis. These cells displayed multiple behaviors with two distinct populations of cells apparent: one with a constrained pattern of migration and one with a highly migratory subset. The proportion of these populations varied over time associated with changes in antigen availability as well as T cell expression of the inhibitory receptor PD1. Read More

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http://dx.doi.org/10.1016/j.immuni.2008.12.013DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2696229PMC
February 2009
16 Reads
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