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http://dx.doi.org/10.5483/BMBRep.2019.52.4.271

Interleukin-2/antibody complex expanding Foxp3+ regulatory T cells exacerbates Th2-mediated allergic airway inflammation  

Hong, Sung-Wook (Academy of Immunology and Microbiology, Institute for Basic Science (IBS))
O, Eunju (Academy of Immunology and Microbiology, Institute for Basic Science (IBS))
Lee, Jun Young (Academy of Immunology and Microbiology, Institute for Basic Science (IBS))
Yi, Jaeu (Academy of Immunology and Microbiology, Institute for Basic Science (IBS))
Cho, Kyungjin (Academy of Immunology and Microbiology, Institute for Basic Science (IBS))
Kim, Juhee (Academy of Immunology and Microbiology, Institute for Basic Science (IBS))
Kim, Daeun (Academy of Immunology and Microbiology, Institute for Basic Science (IBS))
Surh, Charles D. (Academy of Immunology and Microbiology, Institute for Basic Science (IBS))
Kim, Kwang Soon (Academy of Immunology and Microbiology, Institute for Basic Science (IBS))
Publication Information
BMB Reports / v.52, no.4, 2019 , pp. 283-288 More about this Journal
Abstract
$Foxp3^+$ regulatory $CD4^+$ T (Treg) cells play an essential role in preventing overt immune responses against self and innocuous foreign antigens. Selective expansion of endogenous Treg cells in response to the administration of interleukin (IL)-2/antibody complex, such as the IL-2/JES6-1 complex (IL-2C) in mice, is considered an attractive therapeutic approach to various immune disorders. Here, we investigated the therapeutic potential of IL-2C in allergic airway inflammation models. IL-2C treatment ameliorated Th17-mediated airway inflammation; however, unexpectedly, IL-2C treatment exacerbated Th2-mediated allergic airway inflammation by inducing the selective expansion of Th2 cells and type-2 innate lymphoid cells. We also found that IL-2 signaling is required for the expansion of Th2 cells in lymphoproliferative disease caused by Treg cell depletion. Our data suggest that IL-2C is selectively applicable to the treatment of allergic airway diseases depending on the characteristics of airway inflammation.
Keywords
Airway inflammation; $Foxp3^+$ regulatory T cell; IL-2/antibody complex; Th17; Th2;
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