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Infection drives long-term meningeal engraftment by inflammatory monocytes that impair central nervous system immunity [I]

ABSTRACT: Infection drives long-term meningeal engraftment by inflammatory monocytes that impair central nervous system immunity [I]

PROVIDER: PRJNA427333 | ENA |

REPOSITORIES: ENA

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Infection drives long-term meningeal engraftment by inflammatory monocytes that impair central nervous system immunity

Project description:Infection drives long-term meningeal engraftment by inflammatory monocytes that impair central nervous system immunity

| PRJNA428167 | ENA

Infection drives long-term meningeal engraftment by inflammatory monocytes that impair central nervous system immunity [II]

Project description:Tissue-resident macrophages have an embryonic origin, but are replenished under steady state conditions in some tissues by blood monocytes that can adopt genotypic and phenotypic features of the residents. However, little is known about the residency and functional properties of infiltrating macrophages after an inflammatory challenge. The meninges of the central nervous system (CNS) are populated by a dense network of specialized macrophages that act as resident immune sentinels. Here we show that following lymphocytic choriomeningitis virus infection resident meningeal macrophages become activated by innate inflammatory cytokines, acquire viral antigen, and interact directly with infiltrating cytotoxic T lymphocytes (CTL), which leads to their depletion. Concurrently, the meninges are heavily infiltrated by peripherally-derived inflammatory monocytes that engraft the meningeal niche and remain in situ for months after viral clearance. This engraftment leads to phenotypic and functional changes in the pool of resident meningeal macrophages that depends in part on IFNγ signaling. These changes include loss of bacterial and immunoregulatory sensors that impede subsequent CNS immune reactions. Collectively, these data indicate that peripheral monocytes can engraft the meninges after an inflammatory challenge, imprinting the compartment with long-term defects in immune function.

2019-03-06 | GSE108647 | GEO

Infection drives long-term meningeal engraftment by inflammatory monocytes that impair central nervous system immunity [I]

2019-03-06 | GSE108467 | GEO

Infection drives long-term meningeal engraftment by inflammatory monocytes that impair central nervous system immunity [II]

Project description:Infection drives long-term meningeal engraftment by inflammatory monocytes that impair central nervous system immunity [II]

| PRJNA428169 | ENA

Infection drives long-term meningeal engraftment by inflammatory monocytes that impair central nervous system immunity

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-03-06 | GSE108648 | GEO

Tumor cells impair immunological synapse formation via central nervous system-enriched metabolite

Project description:Tumor cells impair immunological synapse formation via central nervous system-enriched metabolite

| PRJNA1073468 | ENA

Tumor cells impair immunological synapse formation via central nervous system-enriched metabolite

Project description:Tumor cells impair immunological synapse formation via central nervous system-enriched metabolite

| PRJNA976338 | ENA

Infection drives meningeal engraftment by inflammatory monocytes that impairs CNS immunity.

Project description:Tissue macrophages have an embryonic origin and can be replenished in some tissues under steady-state conditions by blood monocytes. However, little is known about the residency and properties of infiltrating monocytes after an inflammatory challenge. The meninges of the central nervous system (CNS) are populated by a dense network of macrophages that act as resident immune sentinels. Here we show that, following lymphocytic choriomeningitis virus infection, resident meningeal macrophages (MMs) acquired viral antigen and interacted directly with infiltrating cytotoxic T lymphocytes, which led to macrophage depletion. Concurrently, the meninges were infiltrated by inflammatory monocytes that engrafted the meningeal niche and remained in situ for months after viral clearance. This engraftment led to interferon-γ-dependent functional changes in the pool of MMs, including loss of bacterial and immunoregulatory sensors. Collectively, these data indicate that peripheral monocytes can engraft the meninges after an inflammatory challenge, imprinting the compartment with long-term defects in immune function.

| S-EPMC6481670 | biostudies-literature

Iodine I 131 Monoclonal Antibody 3F8 in Treating Patients With Central Nervous System Cancer or Leptomeningeal Cancer

Project description:RATIONALE: Radiolabeled monoclonal antibodies, such as iodine I 131 monoclonal antibody 3F8, can find tumor cells and carry tumor-killing substances to them without harming normal cells. This may be an effective treatment for central nervous system cancer or leptomeningeal metastases. PURPOSE: This phase II trial is studying the side effects and how well iodine I 131 monoclonal antibody 3F8 works in treating patients with central nervous system cancer or leptomeningeal cancer.

| 2037925 | ecrin-mdr-crc

Meningeal cells contribute to postnatal cortical neurogenesis.

Project description:Postnatal brain neurogenesis in mammals is believed to be restricted to rare germinative remnants of the neuroepithelium. In this study, we discovered that, in the postnatal brain, a subset of embryonically derived progenitors is present in meningeal substructures. These cells migrate from the meningeal substructures to the retrosplenial and visual motor cortex and differentiate into (electrically) functional integrated neurons. Lineage tracing analysis revealed that this subset of neural progenitors originate largely from PDGFR+ cells. PDGFR-derived cells differentiate mostly into Satb2+ neurons in cortical layers I-IV. Thus, a reservoir of embryonically derived progenitors in the meninges contributes to postnatal cerebral cortical neurogenesis.

2016-11-23 | E-MTAB-4951 | biostudies-arrayexpress

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