Their previous work revealed that ILC2s are a major source of a tissue-healing growth factor called amphiregulin and have the capacity to receive neuronal signals that modulate their function and can impact disease progression and recovery.

In the new study, they demonstrated that the tissue-protective function of ILC2s depends on production of a molecule called adrenomedullin 2 (ADM2) from the enteric nervous system; administering the molecule expanded this group of ILC2s and provided therapeutic benefit in a preclinical model of inflammatory bowel disease, whereas loss of ADM2 signaling exacerbated disease due to the lack of these protective cells.