한빛사논문
- 조회1,274
Seok-Min Kim1,2, Se-Chan Oh1,2, Sun-Young Lee1,3, Ling-Zu Kong1,4, Jong-Hee Lee2,5 and Tae-Don Kim*,1,2,6,7
1Immunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Korea
2Department of Functional Genomics, KRIBB School of Bioscience, Korea University of Science and Technology (UST), Daejeon, Korea
3Division of Life Science, Korea University, Seoul, Korea
4Department of Biochemistry, Chungnam National University, Daejeon, Korea
5National Primate Research Center (NPRC), KRIBB, Cheongju, Korea
6Biomedical Mathematics Group, Institute for Basic Science (IBS), Daejeon, Korea
7Department of Biopharmaceutical Convergence, School of Pharmacy, Sungkyunkwan University, Suwon, Korea
*Corresponding author: Tae-Don Kim
Abstract
N6 -Methyladenosine (m6 A) is the most abundant epitranscriptomic mark and plays a fundamental role in almost every aspect of mRNA metabolism. Although m6 A writers and readers have been widely studied, the roles of m6 A erasers are not well-understood. Here, we investigate the role of FTO, one of the m6 A erasers, in natural killer (NK) cell immunity. We observe that FTO-deficient NK cells are hyperactivated. Fto knockout (Fto-/- ) mouse NK cells prevent melanoma metastasis in vivo, and FTO-deficient human NK cells enhance the antitumor response against leukemia in vitro. We find that FTO negatively regulates IL-2/15-driven JAK/STAT signaling by increasing the mRNA stability of suppressor of cytokine signaling protein (SOCS) family genes. Our results suggest that FTO is an essential modulator of NK cell immunity, providing a new immunotherapeutic strategy for allogeneic NK cell therapies.
논문정보
- Research article
- 2023년 02월 (BRIC 등록일 2023-03-02)
- 국내 연구진
- 생명과학 > 면역학
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