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Journal of Endocrinology (2008) 196, 67-77       DOI: 10.1677/JOE-07-0317
© 2008 Society for Endocrinology
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Expression of membrane progesterone receptors on human T lymphocytes and Jurkat cells and activation of G-proteins by progesterone

 C Dosiou, A E Hamilton1, Y Pang2, M T Overgaard1, S Tulac1, J Dong2, P Thomas2 and L C Giudice1

Division of Endocrinology and Metabolism, Department of Medicine, Stanford University, Stanford, California 94305, USA 1 Department of Obstetrics, Gynecology and Reproductive Sciences, 505 Parnassus Avenue, University of California, San Francisco, California 94143, USA 2 University of Texas at Austin Marine Science Institute, 750 Channel View Drive, Port Aransas, Texas 78373, USA

(Correspondence should be addressed to L C Giudice; Email: giudice{at}obgyn.ucsf.edu)

Although there is significant evidence for progesterone's role as an immunomodulator, nuclear progesterone receptors have not been consistently identified in immune cells. Recently, three new putative membrane progesterone receptors (mPRs), mPR{alpha}, mPRβ, and mPR{gamma} have been described. The objective of this study was to examine whether mPRs are expressed in peripheral blood leukocytes (PBLs) in women of reproductive age, and to further characterize them in T lymphocytes and immortalized T cells (Jurkat cells). Transcripts for mPR{alpha} and mPRβ but not mPR{gamma}, were detected by RT-PCR in PBLs, T lymphocytes, and Jurkat cells. Western blot analysis showed the presence of the mPR{alpha} and mPRβ proteins on cell membranes of T lymphocytes and Jurkat cells. Expression of the mPR{alpha} mRNA was upregulated in the luteal phase of the menstrual cycle in cluster of differentiation (CD)8+, but not in CD4+, T lymphocytes. Radioreceptor assays revealed specific [3H]progesterone binding to T- and Jurkat cell membranes (Kd 4.25 nM) characteristic of steroid membrane receptors. Progesterone activated an inhibitory G-protein (Gi), suggesting that mPRs are coupled to Gi in Jurkat cells. These results suggest a potential novel mechanism for progesterone's immunoregulatory function through activation of mPRs.




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