Modulating ILC2s in Allergic Airway Inflammation for Therapeutic Intervention

While numerous experiments have illuminated the role of acetylcholine (ACh) in allergic airway inflammation, some limitations persist. Many studies have utilized global knockout models and pharmacological interventions, making it challenging to discern whether observed clinical outcomes directly stem from group 2 innate lymphoid cells (ILC2) changes or arise indirectly from other affected tissues or immune cells. In a study published in Frontiers in Allergy, researchers focus on type 2 cytokines (eg, interleukin-4, -5, -9, and -13, released by immune cells like CD4+ type 2 helper T cells and group 2 innate lymphoid cells [ILC2s]) to understand opportunities for neuromodulation of ILC2 responses.

According to researchers, stimulation of the vagus nerve results in the release of ACh, impacting airway function and contributing to conditions such as chronic obstructive pulmonary disease (COPD) and asthma. ACh exhibited dual roles, exacerbating some diseases while attenuating others, depending on the specific context and target receptors.

Overall, the dynamic neuro-regulation of ILC2s in the lungs holds promise for developing immune-targeted therapies at the neural level, offering potential breakthroughs in treating respiratory diseases like asthma.

"Neuronal signals serve as an efficient method used to maintain a balance between ILC2-mediated host protective and pathogenic type 2 inflammation in the lungs of humans and mice. As such, this field warrants further investigation in its potential to generate better immune targeted therapies at the neural level," said researchers.

Reference

Thomas CM, R. Stokes Peebles. Neural regulation of ILC2s in allergic airway inflammation. Frontiers in Allergy. 2023;3. doi:10.3389/falgy.2022.1094259