CD 84 is markedly up‐regulated in K awasaki disease arteriopathy

Summary The major goals of K awasaki disease ( KD ) therapy are to reduce inflammation and prevent thrombosis in the coronary arteries ( CA ), but some children do not respond to currently available non‐specific therapies. New treatments have been difficult to develop because the molecular pathogenesis is unknown. In order to identify dysregulated gene expression in KD CA , we performed high‐throughput RNA sequencing on KD and control CA , validated potentially dysregulated genes by real‐time reverse transcription–polymerase chain reaction ( RT–PCR ) and localized protein expression by immunohistochemistry. Signalling lymphocyte activation molecule CD 84 was up‐regulated 16‐fold ( P  < 0·01) in acute KD CA (within 2 months of onset) and 32‐fold ( P  < 0·01) in chronic CA (5 months to years after onset). CD 84 was localized to inflammatory cells in KD tissues. Genes associated with cellular proliferation, motility and survival were also up‐regulated in KD CA , and immune activation molecules MX 2 and SP 140 were up‐regulated in chronic KD . CD 84, which facilitates immune responses and stabilizes platelet aggregates, is markedly up‐regulated in KD CA in patients with acute and chronic arterial disease. We provide the first molecular evidence of dysregulated inflammatory responses persisting for months to years in CA significantly damaged by KD .