Abstract | PURPOSE: METHODS:
ALCAM levels were measured in the serum of AD patients and AD-induced murine model by ovalbumin treatment. We next investigated transepidermal water loss, clinical score, Th2-immune responses, skin barrier gene expression and T-cell activation using wild-type (WT) and ALCAM deficiency mice. An oxazolone-induced AD-like model was also established and analyzed using WT- and ALCAM-deficient mice. RESULTS: We found that serum ALCAM levels were elevated in pediatric AD patients as well as WT AD mice, whereas Th2-type cytokine production and AD symptoms were suppressed in ALCAM-deficient mice. In addition, CD4⁺ effector T-cell counts in murine skin and skin-draining lymph nodes were lower in ALCAM-deficient mice than in their WT counterparts. ALCAM deficiency was also linked to higher expression of skin barrier genes and number of lamellar bodies. CONCLUSIONS: These findings indicate that ALCAM may contribute to AD pathogenesis by meditating a Th2-dominant immune response and disrupting the barrier function of the skin.
|
Authors | Mi Seon Oh, Jung Yeon Hong, Mi Na Kim, Eun Ji Kwak, Soo Yeon Kim, Eun Gyul Kim, Kyung Eun Lee, Yun Seon Kim, Hye Mi Jee, Seo Hyeong Kim, In Suk Sol, Chang Ook Park, Kyung Won Kim, Myung Hyun Sohn |
Journal | Allergy, asthma & immunology research
(Allergy Asthma Immunol Res)
Vol. 11
Issue 5
Pg. 677-690
(Sep 2019)
ISSN: 2092-7355 [Print] Korea (South) |
PMID | 31332979
(Publication Type: Journal Article)
|
Copyright | Copyright © 2019 The Korean Academy of Asthma, Allergy and Clinical Immunology · The Korean Academy of Pediatric Allergy and Respiratory Disease. |