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International Immunology Advance Access published online on October 27, 2007
International Immunology, doi:10.1093/intimm/dxm107
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© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Spleen B cells from BALB/c are more prone to activation than spleen B cells from C57BL/6 mice during a secondary immune response to cruzipain

Andrea Pellegrini1, Natalia Guiñazú1, Maria Pilar Aoki1, Isabel Chico Calero2, Eugenio Antonio Carrera-Silva1, Nuria Girones2, Manuel Fresno2 and Susana Gea1

1 Inmunología, Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, CIBICI-CONICET, Universidad Nacional de Córdoba, Córdoba, Argentina
2 Centro de Biología Molecular Severo Ochoa, CSIC-Universidad Autónoma de Madrid, España

Correspondence to: Correspondence to: S. Gea; E-mail: sgea{at}mail.fcq.unc.edu.ar

There is an increasing interest in the study of roles that B cells may play in regulating immune responses both in protection and in pathogenesis. However, little is known about additional immune functions of B cells independently of antibody production. In this study, we have assessed how the immunization with T-dependent antigens in different host genetic backgrounds affects several parameters of B cells during secondary immune responses. We have previously reported that BALB/c immunized with cruzipain, induced heart autoimmunity, whereas C57BL/6 mice were resistant. In a comparative study employing the same experimental model, we demonstrated that BALB/c-enriched spleen B cells presented higher ability to proliferate releasing elevated levels of IL-4. Moreover, spleen of immune BALB/c mice presented an increased number of germinal center and plasma cells as well as higher expression of B-cell activation markers (MHC class II, CD40, CD86). These findings demonstrate the influence of genetic background on B-cell activation and emphasize the importance of examining B-cell behavior in the context of the specific immunogens.

Keywords: animal models, B cells, cytokines

Transmitting editor: S. Izui

Received 11 April 2007, accepted 1 October 2007.


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