Single-Cell Profiling of Cells in the Lung of a Patient with Chronic Hypersensitivity Pneumonitis Reveals Inflammatory Niche with Abundant CD39+ T Cells with Functional ATPase Phenotype: A Case Study

Int J Mol Sci. 2023 Sep 22;24(19):14442. doi: 10.3390/ijms241914442.

Abstract

This study investigated immune cell characteristics in chronic hypersensitivity pneumonitis (HP), focusing on CD39-expressing cells' impact on inflammation and tissue remodelling. Lung tissue from an HP patient was analysed using single-cell transcriptomics, flow cytometry, and gene expression profiling. The tissue revealed diverse cell types like macrophages, T cells, fibroblasts, and regulatory T cells (Tregs). CD39-expressing Tregs exhibited heightened ATP hydrolysis capacity and regulatory gene expression. CD39hi cells displayed markers of both Tregs and proinflammatory Th17 cells, suggesting transitional properties. Communication networks involving molecules like SPP1, collagen, CSF1, and IL-1β were identified, hinting at interactions between cell types in HP pathogenesis. This research provides insights into the immune response and cell interactions in chronic HP. CD39-expressing cells dual nature as Tregs and Th17 cells suggests a role in modulating lung inflammation, potentially affecting disease progression. These findings lay the groundwork for further research, underscoring CD39-expressing cells as potential therapeutic targets in HP.

Keywords: CD39; chronic hypersensitivity pneumonitis; regulatory T cells; single-cell transcriptomics.

Publication types

  • Case Reports

MeSH terms

  • Adenosine Triphosphatases / metabolism
  • Alveolitis, Extrinsic Allergic* / pathology
  • Antigens, CD* / metabolism
  • Humans
  • Lung / metabolism
  • Phenotype
  • Single-Cell Analysis
  • T-Lymphocytes, Regulatory

Substances

  • Adenosine Triphosphatases
  • Antigens, CD

Grants and funding

This research was funded by The Common Good, an initiative of The Prince Charles Hospital Foundation. TDS was supported by a PhD Scholarship from The Common Good. BOS was supported by a Fellowship and Team grant from The Common Good.