The innate immune system of rheumatoid arthritis patients was activated, so the macrophages involved in it released the pro-inflammatory factors TNF, IL-1β, IL-8, and the inflammatory process indicated that the nlrp3 inflammasome was abnormally activated, which possibly drove the stimulation of adaptive immunity, potentially leading to autoimmune production (34, 35). Here, IL1B is linked to rheumatoid arthritis.