Activated Leukocyte Cell Adhesion Molecule Modulates Th2 Immune Response in Atopic Dermatitis
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.
Allergy, Asthma & Immunology Research
; : 677-690, 2019.
Artículo
en Inglés
| WPRIM | ID: wpr-762154
PURPOSE:
Activated leukocyte cell adhesion molecule (ALCAM), a member of the immunoglobulin superfamily, is highly expressed on dendritic cells. ALCAM and its receptor CD6 are co-stimulatory molecules in the immunological synapse; their interaction is required for T cell activation. While atopic dermatitis (AD) is recognized as a T helper 2 (Th2)-mediated allergic disease, the role of ALCAM in its pathogenesis is unclear.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.
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