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Updated: Aug 13, 2026
Isolation of Murine Lymph Node Stromal Cells
Published on: August 19, 2014
Expression of prolactin receptors in murine lymphoid cells in normal and autoimmune situations
M C Gagnerault1, P Touraine, W Savino
1CNRS URA 1461, Hôpital Necker, Paris, France.
Insights
Prolactin receptors (PRL-R) are widely expressed on murine immune cells, with expression levels varying by cell type and activation state. Altered PRL-R expression in autoimmune mice suggests a role in disease pathogenesis.
Area of Science:
- Immunology
- Endocrinology
- Cell Biology
Background:
- Prolactin receptors (PRL-R) mediate the effects of prolactin, a hormone implicated in immune system regulation.
- Understanding PRL-R expression on immune cells is crucial for elucidating prolactin's role in both normal physiology and disease states.
Purpose of the Study:
- To comprehensively analyze the expression patterns of PRL-R on various murine lymphoid and hematopoietic cells.
- To investigate the modulation of PRL-R expression upon immune cell activation.
- To explore the potential involvement of PRL-R dysregulation in autoimmune diseases.
Main Methods:
- Flow cytometry using biotinylated anti-PRL-R monoclonal antibodies.
- Polymerase chain reaction (PCR) amplification.
- Analysis of lymphoid cell populations using standard cell surface markers.
- Investigation of PRL-R expression in normal mice and the autoimmune NZB mouse model.
Main Results:
- PRL-R are universally expressed on normal rat and mouse hematopoietic tissues, with high percentages in primary lymphoid organs (thymus, bone marrow).
- Peripheral lymphoid organs show varied PRL-R expression, with strong expression on B cells and macrophages, and moderate expression on T cells (CD4+ and CD8+).
- T cell activation with Concanavalin A (Con A) enhances PRL-R density on cell membranes.
- NZB autoimmune mice exhibit increased PRL-R-bearing T cells and density with age, contrasting with normal mice.
Conclusions:
- PRL-R are widely distributed across murine immune cells, indicating a broad role for prolactin signaling in immunity.
- PRL-R expression is dynamic and can be modulated by immune cell activation.
- Aberrant PRL-R expression in autoimmune-prone mice suggests a link between prolactin signaling and autoimmune disease pathogenesis.
Abstract:
We have analyzed the expression of prolactin receptors (PRL-R) on murine lymphoid cells by using flow cytofluorometry analysis with biotinylated anti-PRL-R mAb raised against several epitopes of the extracellular domain of the PRL-R and by using polymerase chain reaction amplification. We demonstrated that PRL-R were universally expressed in normal rat and mouse hematopoietic tissues. In both primary lymphoid organs, namely, thymus and bone marrow, > 90% of cells were labeled by the anti-PRL-R mAb, but the density of PRL-R (assessed by fluorescence intensity) was lower on thymocytes than on bone marrow cells. In peripheral lymphoid organs there were smaller proportions of cells bearing PRL-R and we could clearly distinguish cell subsets of various fluorescence intensities. By using classical markers for lymphoid cell populations, we noted that all B cells and macrophages from spleen, lymph nodes, and blood strongly expressed the PRL-R. Regarding T cell populations, large proportions (> 85%) of PRL-R+ cells were detected in the four thymocyte subsets, thus contrasting with the smaller proportions (50 to 65%) of T cells labeled in the periphery. Similar percentages of PRL-R+ cells were observed in CD4+ and CD8+ peripheral lymphocyte subsets. Importantly, the stimulation of thymocytes and spleen cells with the T cell mitogen Con A promoted an enhancement of the density of PRL-R molecules on the cell membranes. Because hyperprolactinemia is associated with some autoimmune diseases, we also investigated PRL-R expression in the NZB autoimmune mouse. In contrast to the pattern observed in normal animals, the frequencies of PRL-R-bearing T cells as well as the density of PRL-R per cell increased with age in NZB mice, suggesting that some imbalances of PRL/PRL-R interaction might occur in autoimmune situations. In conclusion, our data provide a molecular basis for a better understanding on the mode of action of PRL within the immune system in physiologic and pathologic situations.
