ArticleEuropean journal of immunology2006
CNS viral infection diverts homing of antibody-secreting cells from lymphoid organs to the CNS.
Article in European journal of immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed, 76 citations in OpenAlex.
- The slow progression of Japanese encephalitis in aged mice is likely associated to B cell recruitment in the brain.Virologica Sinica · 2025Article
- Age-Stratified Treg Responses During Viral Infections of the Central Nervous System: A Literature Review.Journal of medical virology · 2025Review
- Intracranial AAV administration dose-dependently recruits B cells to inhibit the AAV redosing.Molecular therapy. Methods & clinical development · 2025Article
- Immunological findings of West Caucasian bat virus in an accidental host.Journal of virology · 2025Article
- Plasma cells in and around the central nervous system.Frontiers in immunology · 2025Review
- Article
- Further characterization ofFrontiers in immunology · 2023Article
- B cells going viral in the CNS: Dynamics, complexities, and functions of B cells responding to viral encephalitis.Immunological reviews · 2022Review
- B cells in central nervous system disease: diversity, locations and pathophysiology.Nature reviews. Immunology · 2022Review
- Evaluating the role of chemokines and chemokine receptors involved in coronavirus infection.Expert review of clinical immunology · 2022Article
- Viral mouse models used to study multiple sclerosis: past and present.Archives of virology · 2021Review
- B Cells in Multiple Sclerosis and Virus-Induced Neuroinflammation.Frontiers in neurology · 2020Review
- Dynamics of Virus-Specific Memory B Cells and Plasmablasts following Viral Infection of the Central Nervous System.Journal of virology · 2019Article
- Protective Humoral Immunity in the Central Nervous System Requires Peripheral CD19-Dependent Germinal Center Formation following Coronavirus Encephalomyelitis.Journal of virology · 2017Article
- Review
- Activated GL7Brain, behavior, and immunity · 2017Article
- Interferon gamma modulation of disease manifestation and the local antibody response to alphavirus encephalomyelitis.The Journal of general virology · 2016Article
- CXCL13 promotes isotype-switched B cell accumulation to the central nervous system during viral encephalomyelitis.Brain, behavior, and immunity · 2016Article
- CD8+ T cells complement antibodies in protecting against yellow fever virus.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Progression from IgD+ IgM+ to isotype-switched B cells is site specific during coronavirus-induced encephalomyelitis.Journal of virology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Neurotropic coronavirus infection of mice results in acute encephalomyelitis followed by viral persistence. Whereas cellular immunity controls acute infection, humoral immunity regulates central nervous system (CNS) persistence. Maintenance of serum Ab was correlated with tissue distribution of virus-specific Ab-secreting cells (ASC). Although virus-specific ASC declined in cervical lymph node and spleen after infectious virus clearance, virus-specific serum Ab was sustained at steady levels, with a delay in neutralizing Ab. Virus-specific ASC within the CNS peaked rapidly 1 wk after control of infectious virus and were retained throughout chronic infection, consistent with intrathecal Ab synthesis. Surprisingly, frequencies of ASC in the BM remained low and only increased gradually. Nevertheless, virus-specific ASC induced by peripheral infection localized to both spleen and BM. The data suggest that CNS infection provides strong stimuli to recruit ASC into the inflamed tissue through sustained up-regulation of the CXCR3 ligands CXCL9 and CXCL10. Irrespective of Ag deprivation, CNS retention of ASC coincided with elevated BAFF expression and ongoing differentiation of class II+ to class II-CD138+CD19+ plasmablasts. These results confirm the CNS as a major ASC-supporting environment, even after resolution of viral infection and in the absence of chronic ongoing inflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.