Choulaki and colleagues (2015) found that whole blood cell samples from human RA patients stimulated through TLR3 and TLR4 but not TLR2 had increased expression of NLRP3 and higher levels of IL-1β that was driven by caspase-1 and caspase-8 when compared to healthy controls [67]. Here, IL1B is linked to rheumatoid arthritis.