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The immune and nervous systems communicate bidirectionally to maintain tissue homeostasis and regulate physiological functions. A research team led by Dr. Ya-Jen Chang, the Research Fellow of Institute of Biomedical Sciences (IBMS), Academia Sinica, found that respiratory syncytial virus (RSV) infection activates group 2 innate lymphoid cells (ILC2s), prompting them to release serotonin, which exacerbates airway hyperreactivity (AHR) and airway inflammation. Moreover, serotonin released by ILC2s activates vagal sensory neurons (VSNs), contributing to cough hypersensitivity.

Genetic and pharmacological approaches further demonstrated that disrupting ILC2-mediated serotonergic signaling in either ILC2s or VSNs attenuated RSV-induced AHR, airway inflammation, and cough responses.

The study reveals a new role for ILC2s, showing that serotonin release allows these immune cells to “talk” with sensory neurons in the lung. These findings provide new insights into how RSV infection exacerbates cough in asthma and highlight the ILC2-serotonin-neural signaling axis as a potential target for future therapeutic strategies.

This study was supported by Academia Sinica and the National Science and Technology Council, with the first author Chia-Hui Luo, a PhD student from the Taiwan International Graduate Program in Molecular Medicine, Academia Sinica, in collaboration with Dr. Chih-Cheng Chen of IBMS, Academia Sinica, Dr. Alan Chuan-Ying Lai of Taipei Medical University, Dr. Wei-Chang Huang of Taichung Veterans General Hospital, Dr. Wei-Yu Chen of National Cheng Kung University, and Dr. Nicholas W. Lukacs of the University of Michigan, USA. This study was published in Immunity on September 7^th, 2026.