PeproTech Inc.
Originally published online as doi:10.1189/jlb.0407214 on July 5, 2007

Published online before print July 5, 2007
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
jlb.0407214v1
82/5/1027    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Montes, C. L.
Right arrow Articles by Gruppi, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Montes, C. L.
Right arrow Articles by Gruppi, A.
(Journal of Leukocyte Biology. 2007;82:1027-1032.)
© 2007 by Society for Leukocyte Biology

Polyclonal B cell activation in infections: infectious agents’ devilry or defense mechanism of the host?

Carolina L. Montes, Eva V. Acosta-Rodríguez, Maria Cecilia Merino, Daniela A. Bermejo and Adriana Gruppi1

Department of Clinical Biochemistry, School of Chemical Science, National University of Córdoba, Córdoba, Argentina

1 Correspondence: CIBICI, Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Haya de la Torre y Medina Allende, Ciudad Universitaria, 5000 Córdoba, Argentina. E-mail: agruppi{at}mail.fcq.unc.edu.ar

Polyclonal B cell activation is not a peculiar characteristic to a particular infection, as many viruses, bacteria, and parasites induce a strong polyclonal B cell response resulting in hyper-{gamma}-globulinemia. Here, we discuss the different roles proposed for polyclonal B cell activation, which can be crucial for early host defense against rapidly dividing microorganisms by contributing antibodies specific for a spectrum of conserved structures present in the pathogens. In addition, polyclonal B cell activation can be responsible for maintenance of memory B cell responses because of the continuous, unrestricted stimulation of memory B cells whose antibody production may be sustained in the absence of the antigens binding-specific BCR. Conversely, polyclonal activation can be triggered by microorganisms to avoid the host-specific, immune response by activating B cell clones, which produce nonmicroorganism-specific antibodies. Finally, some reports suggest a deleterious role for polyclonal activation, arguing that it could potentially turn on anti-self-responses and lead to autoimmune manifestations during chronic infections.

Key Words: microorganisms • cytokines • natural antibodies • immunoglobulin • immunopathology




This article has been cited by other articles:


Home page
 J. Immunol.Home page
A. T. Vaughan, A. Gorringe, V. Davenport, N. A. Williams, and R. S. Heyderman
Absence of Mucosal Immunity in the Human Upper Respiratory Tract to the Commensal Bacteria Neisseria lactamica but Not Pathogenic Neisseria meningitidis during the Peak Age of Nasopharyngeal Carriage
J. Immunol., February 15, 2009; 182(4): 2231 - 2240.
[Abstract] [Full Text] [PDF]