Literature DB >> 24795470

Primary human cytomegalovirus infection induces the expansion of virus-specific activated and atypical memory B cells.

Nicolas Dauby1, Caroline Kummert2, Sandra Lecomte1, Corinne Liesnard3, Marie-Luce Delforge3, Catherine Donner4, Arnaud Marchant5.   

Abstract

BACKGROUND: Although neutralizing antibodies play a central role in the control of cytomegalovirus (CMV) dissemination, little is known about the response of B lymphocytes to primary human CMV infection.
METHODS: The proportion, phenotype, specificity, and functionality of B-cell subsets were studied in a cohort of pregnant women with primary CMV infection. CMV-seronegative pregnant women, as well as CMV-seronegative and CMV-seropositive healthy adults, were included as controls.
RESULTS: Primary CMV infection was associated with a sustained expansion of activated (CD27(+)CD20(+)CD21(low)) and atypical (CD27(-)CD20(+)CD21(low)) memory B cells (MBCs). Both subsets expressed an effector phenotype, and their proportions were correlated with viremia. Activated MBCs expressed high levels of activation markers and included high frequencies of tumor necrosis α (TNF-α)-producing cells, whereas atypical MBCs expressed high levels of inhibitory receptors and had low TNF-α responses. Fluorescent-labeled antigen experiments indicated that activated and atypical MBCs were enriched in CMV-specific cells.
CONCLUSIONS: Primary CMV infection mobilizes a large pool of memory B cells that includes activated and atypical MBCs. The functional regulation of CMV-specific MBCs may limit the production of antibodies and the control of viral dissemination.
© The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

Entities:  

Keywords:  activated memory B cells; atypical memory B cells; cytomegalovirus; primary infection

Mesh:

Year:  2014        PMID: 24795470     DOI: 10.1093/infdis/jiu255

Source DB:  PubMed          Journal:  J Infect Dis        ISSN: 0022-1899            Impact factor:   5.226


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