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MRPGRX2 Antagonist Treatment Prevents Inflammation and Disease in a Mouse Model of Atopic Dermatitis Dataset 1

ABSTRACT: The Mas-Related G-Protein Coupled Receptor X2 (MRGPRX2) is a promiscuous receptor expressed on mast cells that mediates IgE-independent mast cell activation and degranulation in response to a variety of diverse agonists and has been implicated in numerous inflammatory conditions, including atopic dermatitis. We investigated if the small molecule MRGPRX2 antagonist, INCB000262, improves disease phenotype in the house dust mite + Staphylococcus aureus enterotoxin type B (HDM+SEB) mouse model of atopic dermatitis and further characterized mast cell-mediated aspects of disease. MRGPRX2 knock-in mice were sensitized to HDM+SEB and orally dosed once daily with either vehicle or INCB000262 for 4 weeks, and efficacy and skin transcriptional changes evaluated. INCB000262 attenuated HDM+SEB-induced atopic dermatitis in vivo with improvements observed in skin thickness, transepidermal water loss, tissue weight, and overall clinical score. In addition, transcriptome changes induced by HDM+SEB exhibited a mast cell activation signature consistent with human atopic dermatitis lesional skin, which was attenuated by antagonist treatment. Overall, the MRGPRX2 antagonist, INCB000262, attenuated HDM+SEB-induced atopic dermatitis disease phenotypes and mast cell-associated transcriptional changes, supporting further evaluation of INCB000262 as an oral treatment for atopic dermatitis and other mast cell-mediated diseases.

ORGANISM(S): Mus musculus

PROVIDER: GSE293241 | GEO | 2026/04/01

REPOSITORIES: GEO

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MRPGRX2 Antagonist Treatment Prevents Inflammation and Disease in a Mouse Model of Atopic Dermatitis Dataset 2

Project description:The Mas-Related G-Protein Coupled Receptor X2 (MRGPRX2) is a promiscuous receptor expressed on mast cells that mediates IgE-independent mast cell activation and degranulation in response to a variety of diverse agonists and has been implicated in numerous inflammatory conditions, including atopic dermatitis. We investigated if the small molecule MRGPRX2 antagonist, INCB000262, improves disease phenotype in the house dust mite + Staphylococcus aureus enterotoxin type B (HDM+SEB) mouse model of atopic dermatitis and further characterized mast cell-mediated aspects of disease. MRGPRX2 knock-in mice were sensitized to HDM+SEB and orally dosed once daily with either vehicle or INCB000262 for 4 weeks, and efficacy and skin transcriptional changes evaluated. INCB000262 attenuated HDM+SEB-induced atopic dermatitis in vivo with improvements observed in skin thickness, transepidermal water loss, tissue weight, and overall clinical score. In addition, transcriptome changes induced by HDM+SEB exhibited a mast cell activation signature consistent with human atopic dermatitis lesional skin, which was attenuated by antagonist treatment. Overall, the MRGPRX2 antagonist, INCB000262, attenuated HDM+SEB-induced atopic dermatitis disease phenotypes and mast cell-associated transcriptional changes, supporting further evaluation of INCB000262 as an oral treatment for atopic dermatitis and other mast cell-mediated diseases.

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