Neuroimmune interplay during type 2 inflammation: Symptoms, mechanisms, and therapeutic targets in atopic diseases.

Brian Kim, Marc E Rothenberg, Xin Sun, Claus Bachert, David Artis, Raza Zaheer, Yamo Deniz, Paul Rowe, Sonya Cyr

Journal: The Journal of allergy and clinical immunology 2024;153(4):879-893

PMID: 37634890

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Abstract

Type 2 inflammation is characterized by overexpression and heightened activity of type 2 cytokines, mediators, and cells that drive neuroimmune activation and sensitization to previously subthreshold stimuli. The consequences of altered neuroimmune activity differ by tissue type and disease; they include skin inflammation, sensitization to pruritogens, and itch amplification in atopic dermatitis and prurigo nodularis; airway inflammation and/or hyperresponsiveness, loss of expiratory volume, airflow obstruction and increased mucus production in asthma; loss of sense of smell in chronic rhinosinusitis with nasal polyps; and dysphagia in eosinophilic esophagitis. We describe the neuroimmune interactions that underlie the various sensory and autonomic pathologies in type 2 inflammatory diseases and present recent advances in targeted treatment approaches to reduce type 2 inflammation and its associated symptoms in these diseases. Further research is needed to better understand the neuroimmune mechanisms that underlie chronic, sustained inflammation and its related sensory pathologies in diseases associated with type 2 inflammation.

Address: Kimberly and Eric J. Waldman Department of Dermatology, Mark Lebwohl Center for Neuroinflammation and Sensation, Icahn School of Medicine at Mount Sinai, New York, NY. Electronic address: [email protected].; Division of Allergy and Immunology, Department of Pediatrics, Cincinnati Children's Hospital Medical Center and University of Cincinnati College of Medicine, Cincinnati, Ohio.; Department of Pediatrics, University of California, San Diego, Calif.; Department of Otorhinolaryngology, Head and Neck Surgery, University of Muenster, Muenster, Germany; First Affiliated Hospital, Sun Yat-Sen University, International Airway Research Center, Guangzhou, China.; Jill Roberts Institute for Research in Inflammatory Bowel Disease, Friedman Center for Nutrition and Inflammation, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY.; Sanofi, Cambridge, Mass.; Regeneron Pharmaceuticals, Tarrytown, NY.; Sanofi-Aventis, Bridgewater, NJ.

DOI: 10.1016/j.jaci.2023.08.017

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MeSH Terms: Humans, Inflammation, Dermatitis, Atopic, Pruritus, Sinusitis, Asthma