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

Published online before print July 5, 2007
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(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




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