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Asthma is a heterogeneous disease with persistent symptoms and frequent exacerbations, often triggered by respiratory viruses or allergens exposure. Respiratory syncytial virus (RSV) infection-induced mediators interact with immune cells or vagal sensory neurons (VSNs), mediating asthma features such as airway hyperreactivity (AHR) and cough hypersensitivity. Group 2 innate lymphoid cells (ILC2s) are considered as an important mediator in the pathogenesis of asthma. Neuronal signals have emerged as critical factors that modulate ILC2 function, thereby regulating asthma development. However, the immune pathways-mediated serotonergic circuits underlying these responses remain poorly defined. Here, we identified a serotonergic neuroimmune axis in which pulmonary ILC2s express tryptophan hydroxylase-1 (Tph1) and release serotonin via CCAAT/enhancer-binding protein beta (C/EBPβ)-dependent transcription following interleukin (IL)-33 stimulation. Utilizing conditional deletion of Tph1 in ILC2s and adoptive transfer approaches in murine asthmatic models, we demonstrated the contribution of ILC2-derived serotonin in asthma pathogenesis. Mechanistically, we found that serotonin enhanced IL-33-induced IL-5 and IL-13 productions through the 5-HT2A-NF-κB signaling pathway, thereby exacerbating RSV-induced AHR and type 2 lung inflammation. Moreover, we discovered that ILC2s activates VSNs through a serotonin/5-HT3A axis, thereby driving cough hypersensitivity during RSV infection. Using genetically engineered viral tools, we further demonstrated that inhibition of 5-HT3A expression in VSNs attenuates RSV-evoked cough responses. Clinically, TPH1 and serotonin expressions are elevated and correlate with type 2 cytokine levels in asthmatics. Collectively, our study defines an ILC2-intrinsic serotonergic loop that promotes type 2 lung inflammation and contributes to asthma pathophysiology, further highlighting serotonergic signaling as a potential therapeutic target.