Alphavirus-induced encephalomyelitis: antibody-secreting cells and viral clearance from the nervous system.
about
Multiple immune factors are involved in controlling acute and chronic chikungunya virus infectionImmune heterogeneity in neuroinflammation: dendritic cells in the brainPersistent humoral immune responses in the CNS limit recovery of reactivated murine cytomegalovirusProgression from IgD+ IgM+ to isotype-switched B cells is site specific during coronavirus-induced encephalomyelitis.Defining the chemokine basis for leukocyte recruitment during viral encephalitis.Chronic joint disease caused by persistent Chikungunya virus infection is controlled by the adaptive immune response.Glucocorticoid treatment of MCMV infected newborn mice attenuates CNS inflammation and limits deficits in cerebellar development.Investigating the role for IL-21 in rabies virus vaccine-induced immunity.CD8+ T cells complement antibodies in protecting against yellow fever virus.Mice deficient in interferon-gamma or interferon-gamma receptor 1 have distinct inflammatory responses to acute viral encephalomyelitis.The role of B cells and humoral immunity in Mycobacterium tuberculosis infectionNeurological sequelae induced by alphavirus infection of the CNS are attenuated by treatment with the glutamine antagonist 6-diazo-5-oxo-l-norleucineRecruitment and retention of B cells in the central nervous system in response to alphavirus encephalomyelitis.Intrathecal humoral immunity to encephalitic RNA viruses.Immune responses to non-tumor antigens in the central nervous system.Adaptive lymphocyte profiles correlate to brain Aβ burden in patients with mild cognitive impairment.Age has a role in driving host immunopathological response to alphavirus infection.Susceptibility and Lethality of Western Equine Encephalitis Virus in Balb/c Mice When Infected by the Aerosol Route.An optimized method for enumerating CNS derived memory B cells during viral-induced inflammation.Interferon gamma modulation of disease manifestation and the local antibody response to alphavirus encephalomyelitis.Activated GL7+ B cells are maintained within the inflamed CNS in the absence of follicle formation during viral encephalomyelitis.Germline IgM is sufficient, but not required, for antibody-mediated alphavirus clearance from the central nervous system.Death and gastrointestinal bleeding complicate encephalomyelitis in mice with delayed appearance of CNS IgM after intranasal alphavirus infection.CNS InfectionsThe Pathogenesis of Alphaviruses
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P2860
Alphavirus-induced encephalomyelitis: antibody-secreting cells and viral clearance from the nervous system.
description
2011 nî lūn-bûn
@nan
2011 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Alphavirus-induced encephalomy ...... rance from the nervous system.
@ast
Alphavirus-induced encephalomy ...... rance from the nervous system.
@en
type
label
Alphavirus-induced encephalomy ...... rance from the nervous system.
@ast
Alphavirus-induced encephalomy ...... rance from the nervous system.
@en
prefLabel
Alphavirus-induced encephalomy ...... rance from the nervous system.
@ast
Alphavirus-induced encephalomy ...... rance from the nervous system.
@en
P2860
P356
P1433
P1476
Alphavirus-induced encephalomy ...... rance from the nervous system.
@en
P2093
Talibah U Metcalf
P2860
P304
11490-11501
P356
10.1128/JVI.05379-11
P407
P577
2011-08-24T00:00:00Z