An inhibitory immunoreceptor, Allergin-1, suppresses FITC-induced type 2 contact hypersensitivity.

Biochem Biophys Res Commun

Department of Immunology, Faculty of Medicine, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan; Life Science Center for Survival Dynamics, Tsukuba Advanced Research Alliance (TARA), 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan; R&D Center for Innovative Drug Discovery, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan. Electronic address:

Published: November 2021

Although allergic contact dermatitis (ACD) is the most common T cell-mediated inflammatory responses against an allergen in the skin, the pathogenesis of ACD remains incompletely understood. In the sensitization phase in ACD, hapten-bearing dermal dendritic cells (DCs) play a pivotal role in the transport of an antigen to the lymph nodes (LNs), where they present the antigen to naïve T cells. Here we report that Allergin-1, an inhibitory immunoreceptor containing immunoreceptor tyrosine-based inhibitory motif (ITIM) in the cytoplasmic region, is highly expressed on dermal DCs. Mice deficient in Allergin-1 exhibited exacerbated fluorescein isothiocyanate (FITC)-induced type 2 contact hypersensitivity (CHS) such as ear swelling and skin eosinophilia. Allergin-1-deficient mice also showed larger numbers of CD4 T cells and FITC-bearing DCs and greater expressions of type 2 cytokines, including IL-5, IL-10 and IL-13, in the draining LNs than did wild type mice. In sharp contrast, Allergin-1-deficient mice showed comparable level of type 1 CHS induced by 2,4-dinitrofluorobenzene (DNFB). These results suggest that Allergin-1 on dermal DC inhibits type 2, but not type 1, immune responses in the sensitization phase of CHS.

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http://dx.doi.org/10.1016/j.bbrc.2021.09.048DOI Listing

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