Wen Min Zeng, Zong Xian Li, Chao Zhong, Yu Feng Xie, Xiao Qian Yu
Species-specific ILC dynamics underscore distinct immunopathogenic mechanisms: human periodontitis is characterised by the predominance of ILC3s, whereas, in murine disease, there is an association with the loss of ILC2s and an expansion of pro-inflammatory ILC1s/ILC3s. These observations place ILC3s as central mediators in chronic human diseases and emphasise the necessity for therapeutic strategies tailored to target specific ILC subsets.
OBJECTIVE: To characterise the subset dynamics of innate lymphoid cells (ILCs) in human and murine periodontitis to elucidate their roles in disease progression.
METHODS: Human gingival samples were harvested from periodontitis patients and healthy controls. A murine ligature-induced periodontitis model was established. Gingival ILC subsets (ILC1s, ILC2s, ILC3s) were analysed by flow cytometry.
RESULTS: Human periodontitis exhibited elevated total ILCs (from 1.34% to 2.06%) and a pronounced increase in ILC3s (from 0.92% to 29.70%). In mice, 3 days post-ligation, there was a marked decrease in total ILCs (from 10.80% to 0.85%), primarily due to the depletion of ILC2s (from 81.55% to 60.08%), whereas ILC1s (from 1.41% to 15.07%) and ILC3s (from 0.75% to 2.87%) expanded. These changes became even more pronounced 7 days after ligation.
CONCLUSION: Species-specific ILC dynamics underscore distinct immunopathogenic mechanisms: human periodontitis is characterised by the predominance of ILC3s, whereas, in murine disease, there is an association with the loss of ILC2s and an expansion of pro-inflammatory ILC1s/ILC3s. These observations place ILC3s as central mediators in chronic human diseases and emphasise the necessity for therapeutic strategies tailored to target specific ILC subsets.