title: YC-1 enhances natural killer cell differentiation from hematopoietic stem cells.
abstract: NK cells play crucial roles in innate immunity and adaptive immunity. The detailed mechanisms, however, governing NK cell development remains unclear. In this study, we report that YC-1 significantly enhances NK cell populations differentiated from human umbilical cord blood hematopoietic stem cells (HSCs). NK cells increased by YC-1 display both phenotypic and functional features of fully mature NK (mNK) cells, but YC-1 does not affect the activation of mNK cells. YC-1 did not affect cGMP production and phosphorylation of STAT-5 which is essential for IL-15R signaling. On the other hand, YC-1 increased p38 MAPK phosphorylation during NK cell differentiation. Furthermore, p38 inhibitor SB203580 inhibited the differentiation of NK cells enhanced by YC-1. Taken together, these data suggest that YC-1 enhances NK cell differentiation through the activation of p38 MAPK which is involved in NK cell differentiation.
authors.affiliation: Cell Therapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Yuseong-gu, Daejeon 305-806, Republic of Korea.
authors.forename: Sohyun
authors.initials: S
authors.lastname: Yun
authors.forename: Suk Hyung
authors.initials: SH
authors.lastname: Lee
authors.forename: Yun Hee
authors.initials: YH
authors.lastname: Kang
authors.forename: Mira
authors.initials: M
authors.lastname: Jeong
authors.forename: Mi Jeong
authors.initials: MJ
authors.lastname: Kim
authors.forename: Mi Sun
authors.initials: MS
authors.lastname: Kim
authors.forename: Zheng-Hao
authors.initials: ZH
authors.lastname: Piao
authors.forename: Hyun-Woo
authors.initials: HW
authors.lastname: Suh
authors.forename: Tae-don
authors.initials: TD
authors.lastname: Kim
authors.forename: Pyung-Keun
authors.initials: PK
authors.lastname: Myung
authors.forename: Suk-Ran
authors.initials: SR
authors.lastname: Yoon
authors.forename: Inpyo
authors.initials: I
authors.lastname: Choi
mesh_terms: D015153:Blotting, Western; D002454:Cell Differentiation / Q000187:drug effects*; D045744:Cell Line, Tumor; D006152:Cyclic GMP / Q000378:metabolism; D020536:Enzyme Activators / Q000494:pharmacology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005312:Fetal Blood / Q000166:cytology; D005434:Flow Cytometry; D006412:Hematopoietic Stem Cells / Q000187:drug effects*; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D007191:Indazoles / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D007694:Killer Cells, Natural / Q000187:drug effects*; D010766:Phosphorylation; D011725:Pyridines / Q000494:pharmacology; D053647:Receptors, Interleukin-15 / Q000187:drug effects; D050799:STAT5 Transcription Factor / Q000096:biosynthesis; D015398:Signal Transduction / Q000187:drug effects; D048051:p38 Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D020536:Enzyme Activators; D004791:Enzyme Inhibitors; D007093:Imidazoles; D007191:Indazoles; D011725:Pyridines; D053647:Receptors, Interleukin-15; D050799:STAT5 Transcription Factor; C090937:3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole; D048051:p38 Mitogen-Activated Protein Kinases; D006152:Cyclic GMP; C093642:SB 203580