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FABP5 as a possible biomarker in atopic march: FABP5-induced Th17 polarization, both in mouse model and human samples

 Jungsoo Lee  ;  Bomi Kim  ;  Howard Chu  ;  KeLun Zhang  ;  Hyeran Kim  ;  Ji Hye Kim  ;  Seo Hyeong Kim  ;  Youdong Pan  ;  Ji Yeon Noh  ;  ZhengWang Sun  ;  Jongsun Lee  ;  Kyoung Yong Jeong  ;  Kyung Hee Park  ;  Jung-Won Park  ;  Thomas S Kupper  ;  Chang Ook Park  ;  Kwang Hoon Lee 
 EBIOMEDICINE, Vol.58 : 102879, 2020-08 
Journal Title
Issue Date
Atopic dermatitis ; Atopic march ; Fatty-acid-binding protein 5 ; IL-17A ; Th17
Background: While the incidence of patients with atopic dermatitis (AD) with atopic march (AM) showing respiratory allergy is steadily rising, the pathomechanism is still unknown. There are currently no biomarkers to predict progression of AM.

Methods: To explore the mechanism of AM, patients with AD and AM and healthy controls were recruited and RNA microarray, flow cytometry, quantitative real-time polymerase chain reaction, and immunofluorescence staining were performed. We also co-cultured dendritic cells and CD4+T cells with various Dermatophagoides farinae allergen fractions. Cytokine levels were evaluated using enzyme-linked immunosorbent assay.

Findings: Both fatty-acid-binding protein 5 (FABP5) and Th17-related genes were more highly expressed in AM. FABP5 knockdown significantly decreased Th17-inducing cytokines in keratinocytes and IL-17A in T cells from AM patients. Further confirmation was obtained using an AM mice model compared to mice without AM. Der f 1, a major D. farinae allergen, increased FABP5 and IL-17A expression in T cells from AM patients. Higher serum FABP5 levels from AM patients were positively correlated with serum IL-17A levels.

Interpretation: FABP5 expression, possibly enhanced by higher epicutaneous and respiratory sensitization to Der f 1, may directly promote Th17 responses in AD patients with AM. Thus, AM progression can be explained by Th17 reaction induced by FABP5. FABP5 was identified as a potential biomarker in AM.

Funding: This study was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (Ministry of Science and ICT; No. NRF-2017R1A2B4009568), grants of the Korean Health Technology R&D Project, Ministry for Health, Welfare & Family Affairs, and the Republic of Korea (HI13C0010, HI14C1324, HI14C1799).
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Appears in Collections:
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Dermatology (피부과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Chu, Howard(곡원호)
Park, Kyung Hee(박경희) ORCID logo https://orcid.org/0000-0003-3605-5364
Park, Jung Won(박중원) ORCID logo https://orcid.org/0000-0003-0249-8749
Park, Chang Ook(박창욱) ORCID logo https://orcid.org/0000-0003-3856-1201
Lee, Kwang Hoon(이광훈)
Jeong, Kyoung Yong(정경용) ORCID logo https://orcid.org/0000-0001-9887-1426
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