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Int Immunol. 2016 Dec;28(12):605-609. doi: 10.1093/intimm/dxw046. Epub 2016 Nov 8.

Allergin-1 inhibits TLR2-mediated mast cell activation and suppresses dermatitis.

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Department of Immunology, Faculty of Medicine and.
Department of Immunology, Faculty of Medicine and
Life Science Center of Tsukuba Advanced Research Alliance (TARA), University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan.
Research Center of Immunology, Tsukuba Institute, ONO Pharmaceutical Co., Ltd, 17-2 Wadai, Tsukuba, Ibaraki 300-4247, Japan.
Division of Molecular Pathology, Research Institute for Biomedical Science, Tokyo University of Science, 2669 Yamazaki, Noda, Chiba 278-0022, Japan.
Laboratory for Cytokine Regulation, RIKEN Center for Integrative Medical Sciences (IMS), 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan.


TLR2 recognizes cell wall components of Staphylococcus aureus, which colonizes >90% of atopic eczematous skin lesions. The regulatory mechanisms of TLR2 signaling in the skin remain unclear. Allergin-1, an inhibitory immunoglobulin-like receptor containing an ITIM, is expressed on mast cells (MCs) and inhibits IgE-mediated anaphylaxis in mice. Here, we show that Allergin-1 inhibits TLR2-mediated activation of, and inflammatory cytokine production by, MCs in vitro Compared with wild-type mice, Allergin-1-deficient mice showed enhanced ear swelling with enhanced collagen deposition and greater Ly6G+ neutrophil recruitment after intra-dermal injection of Pam2CSK4 into pinnae. Using Mas-TRECK mice, which is an MC deletion system based on il4 enhancer elements, we also demonstrated that Allergin-1 on MCs is responsible for the Pam2CSK4-induced ear swelling. These results suggest that Allergin-1 on skin MCs suppresses TLR2-induced dermatitis.


TLR2; allergin-1; dermatitis; mast cell

[Indexed for MEDLINE]

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