Regulation of chitinase-3-like-1 in T cell elicits Th1 and cytotoxic responses to inhibit lung metastasisopen access
- Authors
- Kim, Do-Hyun; Park, Hong-Jai; Lim, Sangho; Koo, Ja-Hyun; Lee, Hong-Gyun; Choi, Jin Ouk; Oh, Ji Hoon; Ha, Sang-Jun; Kang, Min-Jong; Lee, Chang-Min; Lee, Chun Geun; Elias, Jack A.; Choi, Je-Min
- Issue Date
- Feb-2018
- Publisher
- NATURE PUBLISHING GROUP
- Citation
- NATURE COMMUNICATIONS, v.9, no.1, pp.1 - 14
- Indexed
- SCIE
SCOPUS
- Journal Title
- NATURE COMMUNICATIONS
- Volume
- 9
- Number
- 1
- Start Page
- 1
- End Page
- 14
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/17812
- DOI
- 10.1038/s41467-017-02731-6
- ISSN
- 2041-1723
- Abstract
- Chitinase-3-like-1 (Chi3l1) is known to play a significant role in the pathogenesis of Type 2 inflammation and cancer. However, the function of Chi3l1 in T cell and its clinical implications are largely unknown. Here we show that Chi3l1 expression was increased in activated T cells, especially in Th2 cells. In addition, Chi3l1-deficient T cells are hyper-responsive to TcR stimulation and are prone to differentiating into Th1 cells. Chi3l1-deficient Th1 cells show increased expression of anti-tumor immunity genes and decreased Th1 negative regulators. Deletion of Chi3l1 in T cells in mice show reduced melanoma lung metastasis with increased IFN gamma and TNF alpha-producing T cells in the lung. Furthermore, silencing of Chi3l1 expression in the lung using peptide-siRNA complex (dNP2-siChi3l1) efficiently inhibit lung metastasis with enhanced Th1 and CTL responses. Collectively, this study demonstrates Chi3l1 is a regulator of Th1 and CTL which could be a therapeutic target to enhance anti-tumor immunity.
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