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1.  CD4+CD25+ regulatory T cells reverse established allergic airway inflammation and prevent airway remodeling 
Background
CD4+CD25+ regulatory T cells can inhibit excessive T-cell responses in vivo. We have previously demonstrated that prophylactic administration of CD4+CD25+ regulatory T cells suppresses the development of acute allergen-induced airway inflammation in vivo.
Objective
We sought to determine the effect of therapeutic transfer of CD4+CD25+ regulatory T cells on established pulmonary inflammation and the subsequent development of airway remodeling.
Methods
CD4+CD25+ cells were transferred after the onset of allergic inflammation, and airway challenges were continued to induce chronic inflammation and airway remodeling.
Results
Administration of CD4+CD25+ regulatory T cells reduced established lung eosinophilia, TH2 infiltration, and expression of IL-5, IL-13, and TGF-β. Moreover, subsequent mucus hypersecretion and peribronchial collagen deposition were reduced after prolonged challenge. In contrast, transfer of CD4+CD25+ regulatory T cells had no effect on established airway hyperreactivity either 7 days or 4 weeks after transfer.
Conclusions
In this study we demonstrate for the first time that therapeutic transfer of CD4+CD25+ regulatory T cells can resolve features of chronic allergen-induced inflammation and prevent development of airway remodeling.
doi:10.1016/j.jaci.2008.05.048
PMCID: PMC3389733  PMID: 18672278
Regulatory T cells; TH2 cells; eosinophils; TGF-β; airway remodeling; allergic inflammation
2.  Resolution of airway inflammation and hyperreactivity after in vivo transfer of CD4+CD25+ regulatory T cells is interleukin 10 dependent 
The Journal of Experimental Medicine  2005;202(11):1539-1547.
Deficient suppression of T cell responses to allergen by CD4+CD25+ regulatory T cells has been observed in patients with allergic disease. Our current experiments used a mouse model of airway inflammation to examine the suppressive activity of allergen-specific CD4+CD25+ T cells in vivo. Transfer of ovalbumin (OVA) peptide–specific CD4+CD25+ T cells to OVA-sensitized mice reduced airway hyperreactivity (AHR), recruitment of eosinophils, and T helper type 2 (Th2) cytokine expression in the lung after allergen challenge. This suppression was dependent on interleukin (IL) 10 because increased lung expression of IL-10 was detected after transfer of CD4+CD25+ T cells, and regulation was reversed by anti–IL-10R antibody. However, suppression of AHR, airway inflammation, and increased expression of IL-10 were still observed when CD4+CD25+ T cells from IL-10 gene–deficient mice were transferred. Intracellular cytokine staining confirmed that transfer of CD4+CD25+ T cells induced IL-10 expression in recipient CD4+ T cells, but no increase in IL-10 expression was detected in airway macrophages, dendritic cells, or B cells. These data suggest that CD4+CD25+ T cells can suppress the Th2 cell–driven response to allergen in vivo by an IL-10–dependent mechanism but that IL-10 production by the regulatory T cells themselves is not required for such suppression.
doi:10.1084/jem.20051166
PMCID: PMC1350743  PMID: 16314435
3.  Resolution of airway inflammation and hyperreactivity after in vivo transfer of CD4+CD25+ regulatory T cells is interleukin 10 dependent 
The Journal of experimental medicine  2005;202(11):1539-1547.
Deficient suppression of T cell responses to allergen by CD4+CD25+ regulatory T cells has been observed in patients with allergic disease. Our current experiments used a mouse model of airway inflammation to examine the suppressive activity of allergen-specific CD4+CD25+ T cells in vivo. Transfer of ovalbumin (OVA) peptide-specific CD4+CD25+ T cells to OVA-sensitized mice reduced airway hyperreactivity (AHR), recruitment of eosinophils, and T helper type 2 (Th2) cytokine expression in the lung after allergen challenge. This suppression was dependent on interleukin (IL) 10 because increased lung expression of IL-10 was detected after transfer of CD4+CD25+ T cells, and regulation was reversed by anti-IL-10R antibody. However, suppression of AHR, airway inflammation, and increased expression of IL-10 were still observed when CD4+CD25+ T cells from IL-10 gene-deficient mice were transferred. Intracellular cytokine staining confirmed that transfer of CD4+CD25+ T cells induced IL-10 expression in recipient CD4+ T cells, but no increase in IL-10 expression was detected in airway macrophages, dendritic cells, or B cells. These data suggest that CD4+CD25+ T cells can suppress the Th2 cell-driven response to allergen in vivo by an IL-10-dependent mechanism but that IL-10 production by the regulatory T cells themselves is not required for such suppression.
doi:10.1084/jem.20051166
PMCID: PMC1350743  PMID: 16314435

Results 1-3 (3)