Background: Innate lymphoid cells (ILCs) populate within lymphoid and non-lymphoid tissues. They bridge the gap between the immune system and parenchymal tissues in non-lymphoid organs, ensuring tissue homeostasis and stabilizing immunity. Unlike T-andB-lymphocytes, the adaptive antigen receptors are not present in ILCs. ILCs are essential for host defense against pathogens while promoting the establishment of advantageous species. This review aims to examine the cell biology of ILCs, along with the cytokines they generate, and the current understanding of their likely pathogenic involvement in the initiation of inflammation in Rheumatoid arthritis (RA). Conclusion: Disruption in ILC activation may lead to persistent inflammation. Patients with RA exhibit an aberrant distribution pattern and function of ILCs, which can reverse the immune system's homeostasis to inflammation, indicating ILCs' potential role in the pathophysiology of RA. Athorough analysis of ILC activity and signaling pathways would highlight these cells as possible therapeutic targets for the future.