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KMID : 1225720190110050677
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Allergy, Asthma & Immunology Research : AAIR
2019 Volume.11 No. 5 p.677 ~ p.690
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Activated Leukocyte Cell Adhesion Molecule Modulates Th2 Immune Response in Atopic Dermatitis
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Oh Mi-Seon
Hong Jung-Yeon
Kim Mi-Na
Kwak Eun-Ji
Kim Soo-Yeon
Kim Eun-Gyul
Lee Kyung-Eun
Kim Yun-Seon
Jee Hye-Mi
Kim Seo-Hyeong
Sol In-Suk
Park Chang-Ook
Kim Kyung-Won
Sohn Myung-Hyun
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Abstract
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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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KEYWORD
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ALCAM, CD166, atopic dermatitis, type 2 helper T cells, skin barrier
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