IL1B and arthritic joint disease: Similarly, MyD88-signalling in Meningococcal sepsis has been associated with high serum levels of C5a [53], a pro-inflammatory mediator that enhances TLR4/MyD88-mediated IL-17F production by macrophages [54] and is pathogenic in arthritis [55–57] due to its promotion of proinflammatory cell migration [58] and osteoclastogenesis, particularly in synergism with IL-1β [59].