Presenting Author: Min-Jhen Jheng
, PhD Candidate at Mayo Clin., Arizona
Abstract:
The mechanisms involved in regulating chronic airway inflammation in asthma are not well understood. The goal of this study was to identify and characterize T regulatory (Treg) cell population(s) that play a key role in suppressing type 2 airway inflammation. We found that chronic exposure to Alternaria alternata fungal extract or crude house dust mite (HDM) induced airway eosinophilia and increased type 2 cytokines levels in the airways of naïve C57BL/6 mice. Both ST2+ and ST2- Treg cell (i.e., CD4+ FoxP3+ T cell) populations developed within the lung tissues and airway lumens. Among them, CCR8+ST2+ Treg cells largely expanded after 4 weeks of allergen exposures. CCR8+ST2+ Treg cells highly expressed Pdcd1 (transcript for PD-1)as well as Il10 and suppressed effector CD4+ T cell proliferation more effectively than CCR8- Treg cells in vitro. Anti-IL-10R antibody that was administered during early exposure to the allergens enhanced eosinophilic airway inflammation. Furthermore, mice deficient in CCR8 (i.e., Ccr8-/- mice) showed more robust airway inflammation than wild-type mice when exposed chronically to Alternaria extract or crude HDM. Finally, alveolar macrophages served as a major source of a CCR8 ligand, CCL8. These findings suggest that several Treg cell populations are identified within the lung tissues during type 2 immune response and that among them CCR8+ST2+ Treg cells contribute to controlling chronic airway inflammation.
CCR8+ ST2+ regulatory T cells in lung tissue effectively alleviate type 2 airway inflammation induced by airborne allergens
Category
Poster and Podium (Block Symposium)
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Date: May 5 Presentation Time: 11:30 AM to 12:45 PM Room: Exhibit Hall F1