Acute peritonitis-induced adipose CD127+ ILC1s express PD-L1 and ameliorate inflammation in mice

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. The immune regulatory role of mesenteric adipose tissue (MAT) during acute peritonitis remains elusive. Here, the authors employ a cecal ligation and puncture mouse model and show that a population of CD127− ILC1 migrates from the spleen to the MAT via CXCR3 – CXCL10 axis. In the MAT, these cells upregulate the expression of CD127 and PD-L1 and help preventing the progression towards sepsis, potentially by regulating TNF production by γδ T cells.