About: Central Nervous System Inflammatory Aggregates in the Theiler's Virus Model of Progressive Multiple Sclerosis

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Central Nervous System Inflammatory Aggregates in the Theiler's Virus Model of Progressive Multiple Sclerosis
Creator	Gilli, Francesca Disano, Krista Pachner, Andrew Royce, Darlene Alvarez, Jorge Gommerman, Jen Kerfoot, Steven
Source	PMC
abstract	Persistent central nervous system (CNS) inflammation, as seen in chronic infections or inflammatory demyelinating diseases such as Multiple Sclerosis (MS), results in the accumulation of various B cell subsets in the CNS, including naïve, activated, memory B cells (Bmem), and antibody secreting cells (ASC). However, factors driving heterogeneous B cell subset accumulation and antibody (Ab) production in the CNS compartment, including the contribution of ectopic lymphoid follicles (ELF), during chronic CNS inflammation remain unclear and is a major gap in our understanding of neuroinflammation. We sought to address this gap using the Theiler's murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD) model of progressive MS. In this model, injection of the virus into susceptible mouse strains results in a persistent infection associated with demyelination and progressive disability. During chronic infection, the predominant B cell phenotypes accumulating in the CNS were isotype-switched B cells, including Bmem and ASC with naïve/early activated and transitional B cells present at low frequencies. B cell accumulation in the CNS during chronic TMEV-IDD coincided with intrathecal Ab synthesis in the cerebrospinal fluid (CSF). Mature and isotype-switched B cells predominately localized to the meninges and perivascular space, with IgG isotype-switched B cells frequently accumulating in the parenchymal space. Both mature and isotype-switched B cells and T cells occupied meningeal and perivascular spaces, with minimal evidence for spatial organization typical of ELF mimicking secondary lymphoid organs (SLO). Moreover, immunohistological analysis of immune cell aggregates revealed a lack of SLO-like ELF features, such as cell proliferation, cell death, and germinal center B cell markers. Nonetheless, flow cytometric assessment of B cells within the CNS showed enhanced expression of activation markers, including moderate upregulation of GL7 and expression of the costimulatory molecule CD80. B cell-related chemokines and trophic factors, including APRIL, BAFF, CXCL9, CXCL10, CCL19, and CXCL13, were elevated in the CNS. These results indicate that localization of heterogeneous B cell populations, including activated and isotype-switched B cell phenotypes, to the CNS and intrathecal Ab (ItAb) synthesis can occur independently of SLO-like follicles during chronic inflammatory demyelinating disease.
has issue date	2019-08-02(xsd:dateTime)
bibo:doi	10.3389/fimmu.2019.01821
bibo:pmid	31428102
has license	cc-by
sha1sum (hex)	c513fb0abb1aa50c3323e4f6d311248701f0280b
schema:url	https://doi.org/10.3389/fimmu.2019.01821
resource representing a document's title	Central Nervous System Inflammatory Aggregates in the Theiler's Virus Model of Progressive Multiple Sclerosis
has PubMed Central identifier	PMC6687912
has PubMed identifier	31428102
schema:publication	Front Immunol
resource representing a document's body	covid:c513fb0abb1aa50c3323e4f6d311248701f0280b#body_text
is schema:about of	named entity 'CNS' named entity 'demyelination' named entity 'phenotypes' named entity 'heterogeneous' named entity 'CXCL9' named entity 'subset' named entity 'neuroinflammation' named entity 'murine' named entity 'meningeal' named entity 'Aggregates' named entity 'Central Nervous System' named entity '27S' named entity 'ACTIVATION' named entity '27S' named entity 'PROGRESSIVE MULTIPLE SCLEROSIS' named entity 'EVIDENCE FOR' named entity 'GAP' named entity 'INDUCED' named entity 'SUSCEPTIBLE' named entity 'JOURNAL ' named entity 'VARIOUS' named entity 'MS.' named entity 'ANTIBODY' named entity 'MENINGES' named entity '2C CELL' named entity 'CHRONIC INFECTION' named entity 'PRESENT' named entity 'DRIVING' named entity 'CXCL10' named entity 'OUR' named entity 'PREDOMINANT' named entity 'CELL PROLIFERATION' named entity 'PRODUCTION' named entity 'FOLLICLES' named entity 'CELL AGGREGATES' named entity 'APRIL' named entity 'TRANSITIONAL' named entity 'HETEROGENEOUS' named entity 'FREQUENTLY' named entity 'ACCUMULATION' named entity 'CNS' named entity 'PERSISTENT INFECTION' named entity 'A MAJOR' named entity 'SECRETING' named entity 'SUBSET' named entity 'ASC' named entity 'DEMYELINATING DISEASE' named entity 'IMMUNE CELL' named entity 'LYMPHOID FOLLICLES' named entity 'PHENOTYPES' named entity 'VIRUS' named entity 'VIRUS MODEL' named entity 'MULTIPLE SCLEROSIS' named entity 'MODEL OF' named entity 'AGGREGATES' named entity 'NEUROIMMUNOLOGY' named entity 'CENTRAL NERVOUS SYSTEM' named entity 'INFLAMMATORY' named entity 'LOCALIZED' named entity 'CELL DEATH' named entity 'INCLUDING' named entity 'MATURE' named entity 'SPACE' named entity 'ASSOCIATED WITH' named entity 'B CELL' named entity 'SWITCHED' named entity 'ASSESSMENT' named entity 'LACK' named entity 'CONTRIBUTION' named entity 'IS A' named entity 'UPREGULATION' named entity 'CELL ACCUMULATION' named entity 'ANALYSIS' named entity 'RELATED' named entity 'TYPICAL'

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