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In Vitro Differentiation of Human CD4+FOXP3+ Induced Regulatory T Cells (iTregs) from Naïve CD4+ T Cells Using a TGF-β-containing Protocol
Published on: December 30, 2016
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Foxp3+ regulatory T cells promote lung epithelial proliferation
J R Mock1, B T Garibaldi1, N R Aggarwal1
1Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Mucosal Immunology
|May 23, 2014
Summary
Regulatory T cells (Treg cells) are crucial for lung repair after injury. These Foxp3(+) T(reg) cells promote alveolar epithelial proliferation and enhance recovery from acute respiratory distress syndrome (ARDS).
Area of Science:
- Immunology
- Pulmonary Medicine
- Cell Biology
Background:
- Acute respiratory distress syndrome (ARDS) is a major cause of mortality with limited understanding of its resolution mechanisms.
- Foxp3(+) regulatory T cells (Treg cells) are implicated in resolving lung injury.
- Alveolar epithelial repair is critical for lung recovery post-injury.
Purpose of the Study:
- To investigate the role of Foxp3(+) Treg cells in the resolution of lung injury and epithelial repair.
- To determine the mechanisms by which Treg cells influence alveolar epithelial proliferation.
- To explore the CD103 integrin's involvement in Treg cell-mediated lung repair.
Main Methods:
- Induction of lung injury using intratracheal lipopolysaccharide in a mouse model.
- Depletion of Foxp3(+) Treg cells to assess their impact on epithelial proliferation and recovery.
- Antibody-mediated blockade of CD103 to investigate its role in Treg cell function.
- Assessment of epithelial proliferation in a pneumonectomy model of regenerative alveologenesis.
- Co-culture experiments with primary type II alveolar cells (AT2) and Treg cells.
Main Results:
- Epithelial proliferation and repair were observed following endotoxin-induced lung injury, coinciding with increased lung Treg cells.
- Depletion of Treg cells led to reduced alveolar epithelial proliferation and delayed recovery from lung injury.
- Blockade of CD103 decreased Treg cell numbers and epithelial proliferation rates.
- Treg cells enhanced epithelial proliferation in a pneumonectomy model and directly increased AT2 cell proliferation in a CD103-dependent manner.
Conclusions:
- Foxp3(+) Treg cells play an integral role in the repair of lung epithelium following injury.
- Treg cell-mediated enhancement of epithelial proliferation is dependent on the CD103 integrin.
- These findings reveal a novel mechanism for ARDS resolution involving Treg cells and epithelial repair.
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