Activated Leukocyte Cell Adhesion Molecule Modulates Th2 Immune Response in Atopic Dermatitis
Allergy, Asthma & Immunology Research
; : 677-690, 2019.
Article
in En
| WPRIM
| ID: wpr-762154
Responsible library:
WPRO
ABSTRACT
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.Key words
Full text:
1
Index:
WPRIM
Main subject:
Skin
/
Dendritic Cells
/
Immunoglobulins
/
Water
/
T-Lymphocytes
/
Gene Expression
/
Ovalbumin
/
Activated-Leukocyte Cell Adhesion Molecule
/
Dermatitis, Atopic
/
Immunological Synapses
Type of study:
Prognostic_studies
Limits:
Animals
/
Humans
Language:
En
Journal:
Allergy, Asthma & Immunology Research
Year:
2019
Type:
Article