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Neuroimmune circuits in allergic immunity
Join us for the next session in Genoskin’s webinar series, where we explore how cutaneous sensory neurons may shape allergic inflammation, including neuroimmune signaling, type 2 immune responses, and potential mTORC1-dependent “neuroimmune training” following repeated allergen exposure.
This episode of Genoskin’s webinar series is scheduled for:
📅 September 23rd, 2026
🕗 8 a.m. (PDT) | 11 a.m. (EDT) | 5 p.m. (CET)
Neuroimmune circuits in allergic immunity
The skin is a densely innervated barrier tissue that must continuously interpret environmental exposures, including protease allergens. Dr Sokol’s team has focused on how cutaneous sensory neurons participate in this process, not merely as downstream mediators of itch, but as active regulators of allergic immune initiation. Their findings indicate that protease allergens directly engage sensory neurons, triggering the release of neuropeptides such as substance P, which promotes dendritic cell migration and subsequent type 2 immune priming. This neuronal sensing pathway is further shaped by the local tissue environment: epidermal γδ T cells produce IL-3, which primes IL-3 receptor–expressing sensory neurons and lowers their threshold for allergen detection, creating a bidirectional neuroimmune circuit within the skin.
Building on this framework, recent work from the team suggests that repeated allergen exposure can durably reshape sensory neuron function through mTORC1-dependent metabolic reprogramming, generating a state of “neuroimmune training” that amplifies itch, dendritic cell recruitment, and allergic sensitization upon re-exposure. Together, these studies support a model in which allergic inflammation is shaped by dynamic communication among barrier-resident immune cells, sensory neurons, and environmental allergens. More broadly, they highlight the skin as a powerful system for understanding how human-relevant neuroimmune circuits encode exposure history and influence allergic disease.
A must-attend session for researchers in immunology, allergy, dermatology, neuroscience, and neuroimmune biology exploring how sensory neurons, immune cells, and environmental allergens may shape skin inflammation.
Register now to gain insight into how neuroimmune interactions may influence allergic inflammation and sensitization.
About the speaker:
Dr. Caroline Sokol
Assistant Professor of Medicine at Harvard Medical School & Ragon InstituteDr. Caroline Sokol is a physician-scientist, practicing allergist, and principal investigator at the Ragon Institute of Mass General Brigham, MIT, and Harvard. She is an Assistant Professor of Medicine at Harvard Medical School and an Assistant Physician at Massachusetts General Hospital. Her laboratory investigates how the nervous and immune systems communicate at barrier tissues to regulate allergen sensing, itch, allergic sensitization, and chronic inflammatory disease.
Dr. Sokol’s work has helped define core principles in allergic immunity and peripheral neuroimmunology. During her graduate and postdoctoral training, she demonstrated that the enzymatic activity of cysteine protease allergens can initiate type 2 immunity and identified key cellular pathways, including basophils and CCR8-dependent dendritic cell migration, that promote allergic immune responses. As an independent investigator, her laboratory showed that sensory neurons serve as primary detectors of protease allergens and relay this detection to dendritic cells through neuropeptide-mediated pathways, establishing neurons as upstream regulators of allergic immunity. Her team also identified a cytokine-dependent neuroimmune circuit in which IL-3-producing skin-resident γδ T cells tune sensory neuron responsiveness to environmental allergens.
Current work in the Sokol laboratory focuses on how prior allergen exposure durably reprograms sensory neurons to amplify future immune responses. This work has introduced the concept of metabolic neuroimmune “training,” in which mTORC1-dependent changes in sensory neuron function lower the threshold for allergic sensitization and promote responses to distinct allergens. Dr. Sokol’s research has broad implications for allergic disease, chronic itch, asthma, and atopic dermatitis, and is supported by multiple NIH and foundation awards. She also serves as Associate Program Director of the Stanbury Physician-Scientist Pathway at MGH.
Additional resources on Dr. Sokol’s research:
- Perner C, Flayer CH, Zhu X, Aderhold PA, Dewan ZNA, Voisin T, Camire RB, Chow OA, Chiu IM, Sokol CL. Substance P release by sensory neurons triggers dendritic cell migration and initiates the type-2 immune response to allergens. Immunity. 2020;53(5):1063–1077.e7.
- Flayer CH, Kernin IJ, Matatia PR, Zeng X, Yarmolinsky DA, Han C, Naik PR, Buttaci DR, Aderhold PA, Camire RB, Zhu X, Tirard AJ, McGuire JT, Smith NP, McKimmie CS, McAlpine CS, Swirski FK, Woolf CJ, Villani AC, Sokol CL. A γδ T cell–IL-3 axis controls allergic responses through sensory neurons. Nature. 2024;634: 440–446.
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