Expression of leptin receptors and response to leptin stimulation of human natural killer cell lines
Abstract
We previously reported that deficiency of leptin receptor (Ob-R(-/-), db/db) in mice led to impaired NK cell function. In the present paper, we, for the first time, found that human NK cell lines constitutively expressed leptin receptor (Ob-R), both long form Ob-R (Ob-R(L)) and short form Ob-R (Ob-R(S)), using immunohistochemical method, Western blotting, and RT-PCR assay. Interestingly, IL-2-dependent NK-92 cells proliferated without change in the presence or absence of leptin stimulation, but their cytotoxicity was dose-dependently responsible for leptin stimulation. The IL-2-independent YT cells were dose-dependently responsible for leptin stimulation to manifest rapid proliferation and strong cytotoxicity against tumor targets. In order to explain the mechanisms underlying the leptin function on NK cell lines, we examined the gene expression of cytokines (IL-2, IFNr), cytotoxic-associated molecules (perforin, FasL) and the activation of cytokine signal pathways (STAT1, STAT3). The results demonstrated that leptin activated the phosphorylation of STAT3 and then improved transcription of IL-2 and perforin genes. Our preliminary study indicates that leptin could affect NK cell function and may play an important role in innate immunity.
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Activation of STAT3 promotes transcription of IL-2 and perforin genes, thereby promoting natural killer cell activation.
“Activation of STAT3 also promotes transcription of IL-2 and perforin genes, thereby promoting natural killer cell activation”
From Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 To Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution (2020) · cites this paper as Zhao et al., 2003
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“Activation of STAT3 also promotes transcription of IL-2 and perforin genes, thereby promoting natural killer cell activation, which plays a major role in innate immunity (Zhao et al., 2003).”
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- Authors
- Zhao, Y., Sun, R., You, L., Gao, C., & Tian, Z.
- Affiliations
- University of Science and Technology of China (CN)
- Shandong First Medical University (CN)
- Corresponding author
- Tian, Zhigang
- Venue
- Biochemical and Biophysical Research Communications
- Publisher
- Elsevier BV
- Published
- 2003-01
- Volume
- 300
- Issue
- 2
- Pages
- 247-252
- ISSN
- 0006-291X (ISSN-L)
- OpenAlex
- W2005387606
- Cited by
- 229
- References
- 2
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 5 · 2023: 11 · 2022: 5 · 2021: 13 · 2020: 14 · 2019: 17 · 2018: 9 · 2017: 9 · 2016: 8 · 2015: 15 · 2014: 12 · 2013: 9 · 2012: 7
- FWCI
- 2.81
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biochemical and Biophysical Research Communications (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China
- Chinese Academy of Sciences
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Cell Function and Interaction
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- leptin, leptin receptor, natural killer cells, NK cell cytotoxicity, NK cell proliferation, STAT3 phosphorylation, interleukin-2, perforin, Fas ligand, innate immunity, cytokine signaling, NK-92 cells
- MeSH terms
- Cell Division, Cell Line, Cytotoxicity, Immunologic, DNA-Binding Proteins, Dose-Response Relationship, Drug, Gene Expression Regulation, Humans, Interleukin-2, Killer Cells, Natural, Membrane Glycoproteins, Receptors, Cell Surface, Transcription, Genetic, Trans-Activators, Up-Regulation, K562 Cells, Leptin, STAT3 Transcription Factor, Pore Forming Cytotoxic Proteins, Perforin, Receptors, Leptin
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