한빛사 논문
Yong Sun Lee*, Ji Eun Yu*, Min Ji Kim, Hyeon Joo Ham, Seong Hee Jeon, Jaesuk Yun, Suk-Gil Song, Chong-Kil Lee, Sang Bae Han#, Dong Ju Son# and Jin Tae Hong#
College of Pharmacy and Medical Research Center, Chungbuk National University, Osongsaengmyeong 1-ro 194-21, Osong-eup, Heungduk-gu, Cheongju, Chungbuk, 28160, Republic of Korea
*These authors contributed equally to this work.
#Correspondences: Drs. Jin Tae Hong, Dong Ju Son and Sang Bae Han
Abstract
Atopic dermatitis (AD) is a chronic recurrent inflammatory skin disease that is difficult to treat despite the discovery of various disease targets and development of therapeutics. Previous clinical studies have shown that chitinase 3-like protein 1 (CHI3L1), also known as YKL-40, is associated with the onset and severity of AD.1-3 Recently, CHI3L1 has attracted attention as a new therapeutic target for treating various diseases, including cancer and autoimmune diseases.4 Our gene-disease network analysis also showed CHI3L1 is associated with various diseases, including inflammatory diseases (Figure S1). However, the role of CHI3L1 in AD pathogenesis is not well-understood. Previously, we provided the first direct evidence that inhibition of CHI3L1 by K284-6111, a novel CHI3L1 inhibitor, ameliorates AD-like skin inflammation.5 Here, we further investigated the role of CHI3L1 in AD pathogenesis and its underlying mechanism using CHI3L1 knockout (KO) mice and a CHI3L1-blocking antibody (CHI3L1-Ab), and based on outcomes, propose that a CHI3L1-targeted therapeutic strategy can be used to treat AD.
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