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• W2396553321 abstract "Prolactin has an immunomodulatory effect and has been associated with B-cell-triggered autoimmune diseases, such as systemic lupus erythematosus (SLE). In mice that develop SLE, the PRL receptor is expressed in early bone marrow B-cells, and increased levels of PRL hasten disease manifestations, which are correlated with a reduction in the absolute number of immature B-cells. The aim of this work was to determine the effect of PRL in an in vitro system of B-cell tolerance using WEHI-231 cells and immature B-cells from lupus prone MRL/lpr mice. WEHI-231 cells express the long isoform of the PRL receptor, and PRL rescued the cells from cell death by decreasing the apoptosis induced by the cross-linking of the B-cell antigen receptor (BCR) as measured by Annexin V and active caspase-3. This decrease in apoptosis may have been due to the PRL and receptor interaction, which increased the relative expression of antiapoptotic Bcl-xL and decreased the relative expression of proapoptotic Bad. In immature B-cells from MRL/lpr mice, PRL increased the viability and decreased the apoptosis induced by the cross-linking of BCR, which may favor the maturation of self-reactive B-cells and contribute to the onset of disease." @default.
• W2396553321 created "2016-06-24" @default.
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• W2396553321 date "2016-01-01" @default.
• W2396553321 modified "2023-10-18" @default.
• W2396553321 title "Prolactin Rescues Immature B-Cells from Apoptosis Induced by B-Cell Receptor Cross-Linking" @default.
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• W2396553321 doi "https://doi.org/10.1155/2016/3219017" @default.
• W2396553321 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4894992" @default.
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• W2396553321 hasPublicationYear "2016" @default.
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