Abstract:
:Protective immunity to rotavirus (RV) is primarily mediated by antibodies produced by RV-specific memory B cells (RV-mBc). Of note, most of these cells express IgM, but the function of this subset is poorly understood. Here, using limiting dilution assays of highly sort-purified human IgM(+) mBc, we found that 62% and 21% of total (non-antigen-specific) IgM(+) and RV-IgM(+) mBc, respectively, switched in vitro to IgG production after polyclonal stimulation. Moreover, in these assays, the median cloning efficiencies of total IgM(+) (17%) and RV-IgM(+) (7%) mBc were lower than those of the corresponding switched (IgG(+) IgA(+)) total (34%) and RV-mBc (17%), leading to an underestimate of their actual frequency. In order to evaluate the in vivo role of IgM(+) RV-mBc in antiviral immunity, NOD/Shi-scid interleukin-2 receptor-deficient (IL-2Rγ(null)) immunodeficient mice were adoptively transferred highly purified human IgM(+) mBc and infected with virulent murine rotavirus. These mice developed high titers of serum human RV-IgM and IgG and had significantly lower levels than control mice of both antigenemia and viremia. Finally, we determined that human RV-IgM(+) mBc are phenotypically diverse and significantly enriched in the IgM(hi) IgD(low) subset. Thus, RV-IgM(+) mBc are heterogeneous, occur more frequently than estimated by traditional limiting dilution analysis, have the capacity to switch Ig class in vitro as well as in vivo, and can mediate systemic antiviral immunity.
journal_name
J Viroljournal_title
Journal of virologyauthors
Narváez CF,Feng N,Vásquez C,Sen A,Angel J,Greenberg HB,Franco MAdoi
10.1128/JVI.01466-12subject
Has Abstractpub_date
2012-10-01 00:00:00pages
10829-40issue
19eissn
0022-538Xissn
1098-5514pii
JVI.01466-12journal_volume
86pub_type
杂志文章abstract::RNA plant viruses use various translational regulatory mechanisms to control their gene expression. Translational enhancement of viral mRNAs that leads to higher levels of protein synthesis from specific genes may be essential for the virus to successfully compete for cellular translational machinery. The control elem...
journal_title:Journal of virology
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doi:10.1128/jvi.76.3.1144-1153.2002
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doi:10.1128/JVI.69.5.2946-2953.1995
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pub_type: 杂志文章
doi:10.1128/JVI.00224-15
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doi:10.1128/JVI.67.1.178-188.1993
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.70.9.6502-6507.1996
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.65.7.3530-3537.1991
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journal_title:Journal of virology
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pub_type: 杂志文章
doi:10.1128/jvi.78.7.3704-3709.2004
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.59.3.669-675.1986
更新日期:1986-09-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.65.10.5417-5424.1991
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.65.7.3906-3910.1991
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journal_title:Journal of virology
pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:2003-03-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.11.1.46-53.1973
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journal_title:Journal of virology
pub_type: 杂志文章
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pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.03202-15
更新日期:2016-03-28 00:00:00