CD84 is markedly up-regulated in Kawasaki disease arteriopathy Journal Article

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Authors: Reindel, R; Bischof, J.; Kim, K. Y.; Orenstein, J. M.; Soares, M. B.; Baker, S. C.; Shulman, S. T.; Perlman, E. J.; Lingen, M. W.; Pink, A. J.; Trevenen, C; Rowley, A. H.
Article Title: CD84 is markedly up-regulated in Kawasaki disease arteriopathy
Abstract: The major goals of Kawasaki 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 CD84 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). CD84 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 MX2 and SP140 were up-regulated in chronic KD. CD84, 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.
Journal Title: Clinical and experimental immunology
Volume: 177
Issue: 1
ISSN: 1365-2249; 0009-9104
Publisher: British Society for Immunology  
Journal Place: England
Date Published: 2014
Start Page: 203
End Page: 211
Language: eng
DOI/URL:

10.1111/cei.12327
Notes: LR: 20150701; CI: (c) 2014; GR: R01 HL 63771/HL/NHLBI NIH HHS/United States; GR: R01 HL063771/HL/NHLBI NIH HHS/United States; GR: R21 HL109955/HL/NHLBI NIH HHS/United States; GR: R21 HL109955/HL/NHLBI NIH HHS/United States; JID: 0057202; 0 (Antigens, CD); 0 (Antigens, Nuclear); 0 (CD84 protein, human); 0 (MX2 protein, human); 0 (Myxovirus Resistance Proteins); 0 (RNA, Messenger); 0 (SP140 protein, human); 0 (Transcription Factors); Arterial calcification of infancy; OID: NLM: PMC4089169; OTO: NOTNLM; 2014/03/12 [accepted]; ppublish