bims-maitce Biomed News
on MAIT cells
Issue of 2025–02–02
two papers selected by
Andy E. Hogan, Maynooth University
  1. Development and Functions of MAIT Cells.
  2. MAIT Cell-Mediated Immune Mechanisms of Dialysis-Induced Peritoneal Fibrosis and Therapeutic Targeting.
  1. Annu Rev Immunol. 2025 Jan 29.
    Development and Functions of MAIT Cells.
    Marion Salou, Rafael A Paiva, Olivier Lantz.
      Mucosal-associated invariant T (MAIT) cells are evolutionarily conserved T cells that recognize microbial metabolites. They are abundant in humans and conserved during mammalian evolution, which suggests that they have important nonredundant functions. In this article, we discuss the evolutionary conservation of MAIT cells and describe their original developmental process. MAIT cells exert a wide variety of effector functions, from killing infected cells and promoting inflammation to repairing tissues. We provide insights into these functions and discuss how they result from the context of stimulation encountered by MAIT cells in different tissues and pathological settings. We describe how MAIT cell numbers and features are modified in disease states, focusing mainly on in vivo models. Lastly, we discuss emerging strategies to manipulate MAIT cells for therapeutic purposes.
    DOI:  https://doi.org/10.1146/annurev-immunol-082323-025943
  2. J Am Soc Nephrol. 2025 Jan 28.
    MAIT Cell-Mediated Immune Mechanisms of Dialysis-Induced Peritoneal Fibrosis and Therapeutic Targeting.
    Yuxiang Sun, Qiang Huang, Juan Sun, Hu Zhou, Dandan Guo, Long Peng, Hongchun Lin, Canming Li, Hongli Shang, Tongtong Wang, Yanxu Chen, Yong Huang, Cheng Hu, Zhaoyong Hu, Yan Lu, Hui Peng.
       BACKGROUND: Peritoneal fibrosis is a serious complication of long-term peritoneal dialysis (PD) and abdominal surgeries, yet effective treatments remain elusive. Given the known roles of mucosal-associated invariant T (MAIT) cells in immune responses and fibrotic diseases, we investigated their involvement in PD-induced peritoneal fibrosis to identify potential therapeutic targets.
    METHODS: We employed single-cell RNA sequencing (scRNA-seq) and flow cytometry to characterize the activation and function of peritoneal MAIT cells in patients undergoing long-term PD. Our investigation focused on the molecular pathways activated by these cells, particularly the MHC class I-related protein 1 (MR1)-mediated interaction with mesothelial cells and subsequent activation of the mTORC1 signaling pathway. We further assessed the impact of inhibiting MAIT cells on fibrogenesis using both in vitro models and Mr1 knockout mice.
    RESULTS: Our study revealed that long-term PD significantly enhanced the activation of MAIT cells, particularly the pro-inflammatory MAIT17 subtype. These activated cells contributed to peritoneal fibrogenesis by binding to the MR1 receptor on mesothelial cells, which triggered hyperglycolysis through the mTORC1 pathway, ultimately leading to fibrogenesis. Notably, we demonstrated that blocking the MR1-MAIT interaction, either through genetic knockout or pharmacological inhibition with acetyl-6-formylpterin (Ac-6-FP), effectively mitigated fibrosis.
    CONCLUSIONS: This study identified MAIT cells as crucial drivers of PD-induced peritoneal fibrosis.
    DOI:  https://doi.org/10.1681/ASN.0000000627
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