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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.  Strain-specific requirement for eosinophils in the recruitment of T cells to the lung during the development of allergic asthma 
The Journal of Experimental Medicine  2008;205(6):1285-1292.
Eosinophils have been implicated as playing a major role in allergic airway responses. However, the importance of these cells to the development of this disease has remained ambiguous despite many studies, partly because of lack of appropriate model systems. In this study, using transgenic murine models, we more clearly delineate a role for eosinophils in asthma. We report that, in contrast to results obtained on a BALB/c background, eosinophil-deficient C57BL/6 ΔdblGATA mice (eosinophil-null mice via the ΔDblGATA1 mutation) have reduced airway hyperresponsiveness, and cytokine production of interleukin (IL)-4, -5, and -13 in ovalbumin-induced allergic airway inflammation. This was caused by reduced T cell recruitment into the lung, as these mouse lungs had reduced expression of CCL7/MCP-3, CC11/eotaxin-1, and CCL24/eotaxin-2. Transferring eosinophils into these eosinophil-deficient mice and, more importantly, delivery of CCL11/eotaxin-1 into the lung during the development of this disease rescued lung T cell infiltration and airway inflammation when delivered together with allergen. These studies indicate that on the C57BL/6 background, eosinophils are integral to the development of airway allergic responses by modulating chemokine and/or cytokine production in the lung, leading to T cell recruitment.
doi:10.1084/jem.20071836
PMCID: PMC2413027  PMID: 18490489

Results 1-2 (2)