Suppressor of cytokine signaling 2 regulates IL-15-primed human NK cell function via control of phosphorylated Pyk2 = SOCS2에 의한 인간 자연살해세포의 기능조절

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Title
Suppressor of cytokine signaling 2 regulates IL-15-primed human NK cell function via control of phosphorylated Pyk2 = SOCS2에 의한 인간 자연살해세포의 기능조절
Author(s)
Suk Hyung Lee; Sohyun Yoon; Z H Piao; M Jeong; Dong Oh Kim; Hai Young Jung; J Lee; Mi-Joung Kim; Mi-Sun Kim; J W Chung; Tae-Don KimSuk Ran Yoon; P D Greenberg; In Pyo Choi
Bibliographic Citation
Journal of Immunology, vol. 185, no. 2, pp. 917-928
Publication Year
2010
Abstract
NK cells are capable of killing virus-infected or tumor cells and producing IFN-γ. Resting NK cells, however, have only minimal cytolytic activity and secrete a low level of IFN-γ. The cytokine IL-15 can promote the expression of effector functions by resting NK cells. In this study, we demonstrate that suppressor of cytokine signaling 2 (SOCS2) has a novel role in IL-15-primed human NK cell function. SOCS2 expression was upregulated in NK cells following stimulation with IL-15. During IL-15-mediated NK cell priming, SOCS2 interacted with phosphorylated proline-rich tyrosine kinase 2 (Pyk2) at tyrosine 402 (p-Pyk2Tyr402) and induced the proteasome-mediated degradation of p-Pyk2Tyr402 via ubiquitination. Knockdown of SOCS2 resulted in the accumulation of p-Pyk2Tyr402 and blocked NK cell effector functions. In addition, NK cell cytolytic activity and IFN-γ production were inhibited by overexpression of the wild-type of Pyk2 but not by the overexpression of tyrosine 402 mutant of Pyk2. These results suggest that SOCS2 regulates human NK cell effector functions via control of phosphorylated Pyk2 depending on IL-15 existence.
ISSN
0022-1767
Publisher
Amer Assoc Immunologists
DOI
http://dx.doi.org/10.4049/jimmunol.1000784
Type
Article
Appears in Collections:
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
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