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Advances in Hematology
Volume 2014 (2014), Article ID 854124, 10 pages
http://dx.doi.org/10.1155/2014/854124
Research Article

Persistent Polyclonal B Cell Lymphocytosis B Cells Can Be Activated through CD40-CD154 Interaction

1Centre Universitaire d’Hématologie et d’Oncologie de Québec, CHU de Québec, Hôpital de l’Enfant-Jésus, 1401 18ième rue, Québec, QC, Canada G1J 1Z4
2Héma-Québec, Recherche et Développement, 1070 avenue des Sciences-de-la-Vie, Québec, QC, Canada G1V 5C3
3Département de Biochimie, de Microbiologie et de Bio-Informatique, Pavillon Alexandre-Vachon, 1045 avenue de la Médecine, Bureau 3428, Université Laval, Québec, QC, Canada G1V 0A6

Received 21 July 2014; Revised 19 November 2014; Accepted 20 November 2014; Published 14 December 2014

Academic Editor: Emili Montserrat

Copyright © 2014 Emmanuelle Dugas-Bourdages et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Persistent polyclonal B cell lymphocytosis (PPBL) is a rare disorder, diagnosed primarily in adult female smokers and characterized by an expansion of CD19+CD27+IgM+ memory B cells, by the presence of binucleated lymphocytes, and by a moderate elevation of serum IgM. The clinical course is usually benign, but it is not known whether or not PPBL might be part of a process leading to the emergence of a malignant proliferative disorder. In this study we sought to investigate the functional response of B cells from patients with PPBL by use of an optimal memory B cell culture model based on the CD40-CD154 interaction. We found that the proliferation of PPBL B cells was almost as important as that of B cells from normal controls, resulting in high immunoglobulin secretion with in vitro isotypic switching. We conclude that the CD40-CD154 activation pathway is functional in the memory B cell population of PPBL patients, suggesting that the disorder may be due to either a dysfunction of other cells in the microenvironment or a possible defect in another B cell activation pathway.