Inflammation-induced Generation of Splenic Erythroblast-like Ter-Cells Inhibits the Progression of Acute Lung Injury via Artemin.
Summary
This mechanistic study identifies a previously unrecognized spleen-derived erythroblast-like population (Ter-cells) originating from megakaryocyte-erythroid progenitors that restrains acute lung injury progression via artemin signaling. It reframes ARDS pathobiology by implicating nonleukocyte cells from a distal organ in modulating lung injury.
Key Findings
- Inflammation induces a spleen-derived erythroblast-like Ter-119+ population (Ter-cells) from megakaryocyte-erythroid progenitors.
- Ter-cells inhibit the progression of acute lung injury via an artemin-dependent mechanism.
- Nonleukocyte cells from a distal organ (spleen) contribute to ALI/ARDS pathobiology.
Clinical Implications
While preclinical, artemin-Ter-cell biology suggests potential biomarkers and therapeutic strategies to limit lung injury progression; future translation could inform early intervention in ARDS.
Why It Matters
Reveals a novel nonleukocyte cellular axis and a druggable mediator (artemin) that regulate ALI/ARDS progression, opening avenues for cell- or cytokine-based therapies.
Limitations
- Preclinical findings without human validation
- Details on experimental models and translational dosing are not provided in the abstract
Future Directions
Validate Ter-cells and artemin signaling in human ALI/ARDS cohorts; explore therapeutic augmentation or ex vivo expansion strategies; delineate upstream triggers and trafficking.
Study Information
- Study Type
- Basic/Mechanistic Research
- Research Domain
- Pathophysiology
- Evidence Level
- V - Preclinical mechanistic study identifying a protective cellular pathway in ALI
- Study Design
- OTHER