IL-17A is the most extensively studied IL-17 cytokine in periodontitis, followed by IL-17F.35 IL-17RE specifically binds IL-17C, influencing Th17 cell function and enhancing adaptive immunity against pathogens.36 This is also essential in host mucosal defense against infection by enhancing innate barriers.36 IL-17C stimulates expression of epithelial host defense mechanisms, including hBD2 (DEFB4A), S100A8, CCL20, and the CXCL family,37 all of which were downregulated in our study (Supplementary Table 1). Here, CCL20 is linked to infection.