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Clinical and Developmental Immunology
Volume 2013, Article ID 287469, 11 pages
Research Article

Prolactin Levels Correlate with Abnormal B Cell Maturation in MRL and MRL/lpr Mouse Models of Systemic Lupus Erythematosus-Like Disease

1UIM en Inmunología, Hospital de Pediatría, CMN Siglo XXI, IMSS, 06720 Mexico City, DF, Mexico
2Departamento de Inmunología, ENCB, IPN, 11340 Mexico City, DF, Mexico
3Unidad de Investigación en Virología y Cáncer Hospital Infantil de México Federico Gómez, 06720 Mexico City, DF, Mexico
4Departamento de Investigación Experimental y Bioterio del Instituto Nacional de Ciencias Médicas y Nutrición “Salvador Zubirán”, 14000 Mexico City, DF, Mexico
5UIM en Inmunoquímica, Hospital de Especialidades, CMN Siglo XXI, IMSS, 06720 Mexico City, DF, Mexico

Received 3 July 2013; Accepted 22 September 2013

Academic Editor: Lenin Pavón

Copyright © 2013 Maria Victoria Legorreta-Haquet 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.


Prolactin (PRL) plays an important role in modulating the immune response. In B cells, PRL enhances antibody production, including antibodies with self-specificity. In this study, our aims were to determine the level of PRL receptor expression during bone-marrow B-cell development and to assess whether the presence of high PRL serum concentrations influences absolute numbers of developing populations and disease outcome in lupus-prone murine models. We observed that the PRL-receptor is expressed in early bone-marrow B-cell; the expression in lupus-prone mice, which had the highest level of expression in pro-B cells and immature cells, differed from that in wild-type mice. These expression levels did not significantly change in response to hyperprolactinemia; however, populations of pro-B and immature cells from lupus-prone strains showed a decrease in the absolute numbers of cells with high PRL-receptor expression in response to PRL. Because immature self-reactive B cells are constantly being eliminated, we assessed the expression of survival factor BIRC5, which is more highly expressed in both pro-B and immature B-cells in response to PRL and correlates with the onset of disease. These results identify an important role of PRL in the early stages of the B-cell maturation process: PRL may promote the survival of self-reactive clones.