Regulation of chitinase-3-like-1 in T cell elicits Th1 and cytotoxic responses to inhibit lung metastasis

Do-Hyun Kim, Hong-Jai Park, Sangho Lim, Ja-Hyun Koo, Hong-Gyun Lee, Jin Ouk Choi, Ji Hoon Oh, Sang-Jun Ha, Min-Jong Kang, Chang-Min Lee, Chun Geun Lee, Jack A. Elias and Je-Min Choi ()
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Do-Hyun Kim: College of Natural Sciences, Hanyang University
Hong-Jai Park: Yale University School of Medicine
Sangho Lim: College of Natural Sciences, Hanyang University
Ja-Hyun Koo: College of Natural Sciences, Hanyang University
Hong-Gyun Lee: College of Natural Sciences, Hanyang University
Jin Ouk Choi: College of Natural Sciences, Hanyang University
Ji Hoon Oh: Yonsei University
Sang-Jun Ha: Yonsei University
Min-Jong Kang: Yale University School of Medicine
Chang-Min Lee: Brown University
Chun Geun Lee: Brown University
Jack A. Elias: Brown University
Je-Min Choi: College of Natural Sciences, Hanyang University

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: 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 IFNγ and TNFα-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.

Date: 2018
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DOI: 10.1038/s41467-017-02731-6

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