自己免疫性関節炎におけるTNFα-induced adipose-related protein (TIARP)の新たな作用機序

  • 井上 明日香
    筑波大学医学医療系内科(膠原病・リウマチ・アレルギー)
  • 松本 功
    筑波大学医学医療系内科(膠原病・リウマチ・アレルギー)
  • 田中 陽子
    筑波大学医学医療系内科(膠原病・リウマチ・アレルギー)
  • 住田 孝之
    筑波大学医学医療系内科(膠原病・リウマチ・アレルギー)

書誌事項

タイトル別名
  • Crucial role of TNFα-induced adipose-related protein (TIARP) in the pathogenesis of autoimmune arthritis

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  Rheumatoid arthritis (RA) is a chronic inflammatory disorder with a variable disease outcome, and is characterized by inflammation of multiple joints. Proinflammtory cytokines, such as tumor necrosis factor alpha (TNFα), interleukin-6 (IL-6) are thought to play crucial roles in the pathology of RA. The prognosis of patients with RA has improved significantly with the recent availability of biologics targeting TNFα and IL-6. Immunization of DBA/1 mice with glucose-6-phosphate isomerase (GPI) induces severe acute arthritis. This arthritis can be controlled by TNFα antagonists, suggesting similar etiology to RA. We performed GeneChip analysis using splenocytes of mice with GPI-induced arthritis. Among the arrayed TNFα-related genes, the expression of TNFα-induced adipose-related protein (TIARP) mRNA was the highest. TIARP was detected specifically in joints and spleens of arthritic mice. Among the splenocytes, CD11b+ cells were the main source of TIARP mRNA. STEAP4 (the human ortholog of TIARP) was highly upregulated in joints of patients with RA and especially co-localized with CD68+ macrophages. In this study, we discuss the role of TIARP in the generation of experimental autoimmune arthritis and the possible clinical application of for the treatment of RA.<br>

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