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Volume 14, No 1, Feb 2004

ISSN: 1001-0602 
EISSN: 1748-7838 2018 
impact factor 17.848* 
(Clarivate Analytics, 2019)

Volume 14 Issue 1, February 2004: 67-73

ORIGINAL ARTICLES

Expression of prolactin receptor and response to prolactin stimulation of human NK cell lines

Rui SUN1,2*, Ai Ling LI2*, Hai Ming WEI1, Zhi Gang TIAN1,2

1School of Life Sciences, University of Science and Technology of China, Hefei 230027, Anhui, China.
2Shandong Cancer Biotherapy Center, Shandong Academy of Medical Science, Jinan 250062, Shandong, China.
Correspondence: Zhi Gang Tian(ustctzg@yahoo.com.cn. )

We have previously shown a critical role of prolactin (PRL) during maturation and anti-tumor effects of murine natural killer (NK) cells in vitro and in vivo. We extended that study by exploring the ability of human NK cell lines (NK-92 and YT cell) to express PRL receptor (PRL-R) and to respond to PRL stimulation in vitro. Both human NK cell lines constitutively expressed PRL-R on membrane and mRNA transcripts, NK-92 cells contained higher level of PRL-R than YT cells, which correlated to the enhanced capacity of the cells to proliferate and to lyse target cells in response to PRL stimulation in the presence of trace amount of IL-2 or IL-15 in vitro. Two differences between IL-2 and IL-15 in functioning on human NK cells were for the first time observed. PRL synergized with IL-15 to improve proliferation of NK cells in a dose-dependent manner without double peak manifesting like IL-2. Although PRL enhanced the cytotoxicity of IL-2 or IL-15 activated NK cells, it exerted the function through up-regulating gene expression of perforin without influence of FasL in IL-2-stimulated NK cells, while in IL-15-stimulated NK cells, PRL did the function through up-regulating gene expression of both perforin and FasL but not IFN|?. PRL increased expressions of IL-2R|á on membrane and of IL-2 mRNA in cells, indicating that PRL up-regulated NK cell function by improving positive feedback between IL-2 and IL-2R. The similar results were also observed in network between IL-15 and IL-15R. These data indicate a potential role of PRL in human NK cell modulation.


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