2026-03-17 理化学研究所
腹膜炎発症時の過剰な炎症を負に調節する脂肪組織内ILC1
＜関連情報＞
- https://www.riken.jp/press/2026/20260317_2/index.html
- https://www.nature.com/articles/s41467-026-69100-0
急性腹膜炎によって誘導される脂肪組織のCD127 + ILC1細胞はPD-L1を発現し、マウスの炎症を軽減する Acute peritonitis-induced adipose CD127+ ILC1s express PD-L1 and ameliorate inflammation in mice
Ritsu Nagata,Yuichi Akama,Pedro Goncalves,Nicolas Serafini,Tomoko Kageyama,Masami Kawasumi,Manami Satoh,Motomu Shimaoka,Hiroshi Ohno & Naoko Satoh-Takayama
Nature Communications Published:05 February 2026
DOI:https://doi.org/10.1038/s41467-026-69100-0
Abstract
Peritonitis is an inflammation of the peritoneum primarily caused by gut perforation and consequent bacterial leakage, a known cause of sepsis. Although adipose tissue is recognized as an immunologically active organ, the involvement of adipose tissue innate lymphoid cells (ILC) in regulating peritonitis remains poorly understood. Here, we employ a cecal ligation and puncture mouse model and demonstrate that circulating CD127− group 1 ILC (ILC1) migrate into the mesenteric adipose tissue (MAT) during the inflammatory period of peritonitis. CD127− ILC1s undergo phenotypic changes to become CD127+ ILC1s, resulting in an increased number of CD127+ ILC1s in the MAT. We also show that this population of CD127+ ILC1s expresses PD-L1, exhibits low IFN-γ production, and potentially acts as a negative regulator of TNF production by γδ T cells, thereby controlling acute peritonitis. Our findings suggest that MAT-CD127+ ILC1s play an important regulatory role in acute peritonitis and may represent a potential therapeutic target for sepsis.
