Interestingly therefore, blocking of B7–CD28 interactions has been reported to be sufficient to prevent development of CIA.52 Finally, the strong down-regulation of TLR4 is similarly likely to suppress B-cell activation and plasma cell generation at this site,53 and in this way, disrupt the destructive chronic inflammation resulting from cells in the joint expressing up-regulated levels of TLRs, including TLR454 and responding to damage-associated molecular pattern molecules, such as heat-shock protein 22 and tenascin-C55 found in the synovium of RA patients. The gene discussed is CD80; the disease is rheumatoid arthritis.