Thus, given the important role of spontaneous TLR2 signalling in synovial inflammation in RA [30] and reports that whilst TLR4 can preferentially couple to IL-6/IL-17 signalling, TLR2 signalling primarily results in IL-1β production in mice exposed to Mycoplasma arthritidis mitogen, a superantigen that induces inflammation resulting in arthritis, skin necrosis and shock [62], our microarray findings that TLR2, IL-1β and C5aR all appear to be targets of 12b in macrophages may further explain the differential protective effects of 12b and 11a in CIA. This evidence concerns the gene C5AR1 and arthritic joint disease.