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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Animals, Arthritis, Biomarkers, Cytokines, Dermatitis, Allergic Contact, Disease Models, Animal, Disease Progression, Gene Deletion, Genetic Association Studies, Genetic Predisposition to Disease, Humans, Immunoglobulin E, Inflammation Mediators, Macrophage Activation, Macrophages, Mast Cells, Mice, Mice, Knockout, Receptors, G-Protein-Coupled.
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Does gPR91 deficiency exacerbate allergic contact dermatitis while reducing arthritic disease in mice? Context: Succinate, in addition to its role as an intermediary of the citric acid cycle, acts as an alarmin, initiating and propagating danger signals resulting from tissue injury or inflammatory stimuli. The contribution of this immune sensing pathway to the development of allergic and inflammatory responses is unknown. Ear thickness of wild-type (wt) and Sucnr1-deficient (Sucnr1 We found augmented ACD reactions in Sucnr1
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A deficiency in succinate sensing during mast cell development confers these cells with a hyperactive phenotype. Such a phenomenon does not translate into exacerbation of asthma or mast cell-dependent arthritis. On the contrary, the fact that Sucnr1 Final Decision: yes