論文

査読有り 筆頭著者 責任著者 国際誌
2020年8月27日

Inappropriate activation of invariant natural killer T cells and antigen-presenting cells with the elevation of HMGB1 in preterm births without acute chorioamnionitis.

American Journal of Reproductive Immunology
  • Masahiko Kato
  • ,
  • Yasuyuki Negishi
  • ,
  • Yoshio Shima
  • ,
  • Yoshimitsu Kuwabara
  • ,
  • Rimpei Morita
  • ,
  • Toshiyuki Takeshita

85
1
開始ページ
e13330
終了ページ
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1111/aji.13330

PROBLEM: Acute chorioamnionitis (aCAM) associated with microbial infection is a primary cause of preterm birth (PB). However, recent studies have demonstrated that innate immunity and sterile inflammation are causes of PB in the absence of aCAM. Therefore, we analyzed immune cells in the decidua of early to moderate PB without aCAM. METHOD OF STUDY: Deciduas were obtained from patients with PB at a gestational age of 24+0 to 33+6  weeks without aCAM in pathological diagnosis. The patients were divided into two groups as follows: patients with labor and/or rupture of membrane (ROM) (no aCAM with labor and/or ROM: nCAM-w-LR), and patients without labor and/or ROM (no aCAM without labor and/or ROM: nCAM-w/o-LR). The immune cells and high mobility group box 1 (HMGB1) levels in the decidua were analyzed using flow cytometry. Co-culture of CD56+ cells with dendritic cells (DCs) and macrophages obtained from the decidua was also performed in the presence of HMGB1. RESULTS: The nCAM-w-LR group demonstrated an accumulation of iNKT cells, and increased expression of HMGB1, TLR4, receptors for advanced glycation end products, and CD1d on DCs and macrophages. HMGB1 facilitated the proliferation of iNKT cells co-cultured with DCs and macrophages, which was found to be inhibited by heparin. CONCLUSIONS: Inappropriate activation of innate immune cells and increased HMGB1 expression may represent parturition signs in human pregnancy. Therefore, control of these cells and HMGB1 antigenicity may be represent a potential therapeutic target for the prevention of PB.

リンク情報
DOI
https://doi.org/10.1111/aji.13330
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/32852122
共同研究・競争的資金等の研究課題
自然免疫異常に起因する流早産-自然免疫の制御による新しい流早産治療を目指して
共同研究・競争的資金等の研究課題
無菌性炎症からアプローチする新しい早産の臨床 -新規の診断・治療を模索する-
ID情報
  • DOI : 10.1111/aji.13330
  • PubMed ID : 32852122

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