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

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

Content Provider	Paperity
Author	Legorreta-haquet, Maria Victoria Fuentes-pananá, Ezequiel M. Hernández-gonzález, Rafael Chávez-rueda, Adriana Karina Chávez-sánchez, Luis Blanco-favela, Francisco Arriaga-pizano, Lourdes Tesoro-cruz, Emiliano Flores-fernández, Rocio
Abstract	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.
File Format	HTM / HTML
ISSN	23148861
DOI	10.1155/2013/287469
Journal	Journal of Immunology Research
Volume Number	2013
e-ISSN	23147156
Language	English
Publisher	Hindawi Limited
Publisher Date	2013-11-19
Access Restriction	Open
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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