Immunoregulation of autocrine prolactin: Suppressing the expression of costimulatory molecules and cytokines in T lymphocytes by prolactin receptor knockdown

• Published in: Cellular immunology Vol. 263; no. 1; pp. 71 - 78
• Main Authors: Xu, Dongming, Lin, Ling, Lin, Xiahong, Huang, Ziyang, Lei, Zhenmin
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 2010
• Subjects: Antigens, CD - genetics; Antigens, CD - immunology; Antigens, CD - metabolism; Autocrine Communication - immunology; Autocrine signalling; Bioassay; Cell Proliferation; Cytokines; Cytokines - genetics; Cytokines - immunology; Cytokines - metabolism; Down-Regulation; Gene Knockdown Techniques; Genetic Vectors; Humans; Immunomodulation; Immunoregulation; Jurkat Cells; Lentivirus - genetics; Lymphocyte Activation - genetics; Lymphocytes; Prolactin; Prolactin - immunology; Prolactin - metabolism; Receptor; Receptors, Prolactin - antagonists & inhibitors; Receptors, Prolactin - genetics; Receptors, Prolactin - immunology; Receptors, Prolactin - metabolism; RNA interference; RNA, Small Interfering - genetics; T-Lymphocytes - immunology; T-Lymphocytes - metabolism; T-Lymphocytes - pathology; Bioassay; RNA interference; Cytokines; Prolactin; Receptor; Lymphocytes; Immunoregulation
• ISSN: 0008-8749; 1090-2163; 1090-2163
• DOI: 10.1016/j.cellimm.2010.02.018

Ample evidence indicates that prolactin (PRL) secreted from the pituitary gland plays an important role in a variety of human immune responses. However, the immunoregulation of autocrine PRL in T lymphocytes is not fully understood. To evaluate the role of autocrine PRL in T lymphocyte activation, PRL receptor (PRLR) in Jurkat cells was silenced by lentivirus-mediated stable expression of PRLR shRNAi. Knockdown of PRLR resulted in a considerable reduction of phytohemagglutinin (PHA)-induced T cell proliferation. Moreover, the synthesis and secretion of CD137, CD154, IL-2 and IL-4 were significantly decreased, while the production of CD28, IFN-γ and IL-10 was not affected in PHA-primed PRLR-deficient cells. These results demonstrate the importance of autocrine regulation of the PRL signaling in T lymphocyte growth and activation, and support a mechanism by which autocrine PRL participates in the immunoregulation through selectively influencing the expression of certain critical costimulatory molecules and cytokines.