ArticleJournal of translational medicine2026
Mast cell-specific receptor MrgprB2 selectively mediates oxaliplatin-induced neuropathic pain.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundChemotherapy-induced peripheral neuropathy (CIPN) causes debilitating pain that limits anticancer treatment, yet effective therapies remain limited. Mast cells (MCs) regulate neuroimmune signaling implicated in CIPN, but their receptor-specific contributions remain poorly understood. In mice, oxaliplatin and paclitaxel produce robust mechanical and cold hypersensitivities that mirror CIPN pain. Mas-related G-protein-coupled receptor B2 (MrgprB2) and its human orthologue MrgprX2 are MC-restricted receptors that mediate non-IgE-mediated activation. However, whether MrgprB2 signaling differently contributes to oxaliplatin- versus paclitaxel-induced CIPN pain remains unclear.
methodsWe employed a comparative mechanistic approach using wild-type (WT) and MrgprB2 knockout (KO) mice to define receptor-specific contributions to oxaliplatin- versus paclitaxel-induced CIPN pain. Behavioral assessments of mechanical and cold hypersensitivity were integrated with histological profiling of MC recruitment and mediator profiles. Genetic findings were validated pharmacologically with osthole, a natural MrgprB2/X2 antagonist.
resultsBoth oxaliplatin and paclitaxel induced cutaneous MC accumulation in the hindpaw of WT mice, but they triggered distinct MC mediator-release profiles in vivo: oxaliplatin preferentially elevated tryptase, while paclitaxel was associated with greater histamine enrichment. Yet, neither drug directly activate MCs in vitro, as indicated by unchanged β-hexosaminidase release and calcium signaling. Importantly, MrgprB2 KO selectively attenuated oxaliplatin-induced tryptase upregulation and mechanical and cold hypersensitivity in vivo, without affecting paclitaxel-induced histamine changes or pain behavior. Consistently, with these genetic results, osthole selectively attenuated oxaliplatin-induced pain, but not paclitaxel-induced pain in WT mice.
conclusionsThese findings support a mechanistic dichotomy in CIPN pain, indicating that MrgprB2 contributes selectively to oxaliplatin-induced, but not paclitaxel-induced, CIPN in mice. More broadly, they suggest that CIPN involves mechanistically distinct neuroimmune states depending on the chemotherapeutic class and highlight MrgprB2/X2 as a drug class-selective target for platinum-induced CIPN pain treatment.
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