IL17A and rheumatoid arthritis: In previous studies, inflammatory cells such T lymphocytes, macrophages, neutrophils, as well as other cell types have been shown to release pro-inflammatory proteins, such as TNF-α, IL-17A, and macrophage colony-stimulating factor (M-CSF), and promote clusters of differentiation molecule 11b (CD11b) positive cells, leading to osteoclastogenesis in RA [1,12,13,14].