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10.1016/j.jaci.2016.08.034 http://scihub22266oqcxt.onion/10.1016/j.jaci.2016.08.034 C5378695!5378695!27717665     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Allergy+Clin+Immunol 2017 ; 139 (5): 1468-1477.e2 Nephropedia Template TP {{tp|p=27717665|t=2017. ILC2 Suppression by Regulatory T Cells Attenuates Airway Hyperreactivity and Requires ICOS:ICOS-Ligand Interaction |pdf=|usr=}}{{27717665}} gab.com Text ILC2 Suppression by Regulatory T Cells Attenuates Airway Hyperreactivity and Requires ICOS:ICOS-Ligand Interaction JO: J Allergy Clin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27717665 #FOAvip Background: Atopic diseases including asthma exacerbate type 2 immune responses and involve a number of immune cell types, including regulatory T cells (Tregs) and the emerging group 2 innate lymphoid cells (ILC2s). While ILC2s are potent producers of type 2 cytokines, the regulation of ILC2 activation and function is not well understood. Objective: In the present study, we evaluate for the first time how Tregs interact with pulmonary ILC2s and control their function. Methods: ILC2s and Tregs were evaluated using in vitro suppression assays, cell-contact assays, and gene expression panels. Also, human ILC2s and Tregs were adoptively transferred into NOD SCID gamma-C deficient (NSG) mice, which were given isotype or anti-ICOS-L antibodies, then challenged with IL-33 and assessed for AHR. Results: We show that induced Tregs (iTregs), but not natural Tregs (nTregs), effectively suppress the production of ILC2-driven, pro-inflammatory cytokines IL-5 and IL-13, both in vitro and in vivo. Mechanistically, our data reveal the necessity of Inducible T cell Costimulator (ICOS):ICOS-Ligand cell contact for Treg-mediated ILC2 suppression, alongside suppressive cytokines TGF-? and IL-10. Using a translational approach, we then demonstrate that human iTregs suppress syngeneic human ILC2s via ICOS-L to control airway inflammation in a humanized ILC2 mouse model. Conclusion: These findings suggest that peripheral expansion of induced Tregs may serve as a promising therapeutic target against ILC2-dependent asthma. Twit Text FOAVip ILC2 Suppression by Regulatory T Cells Attenuates Airway Hyperreactivity and Requires ICOS:ICOS-Ligand Interaction ????J Allergy Clin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27717665 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27717665 #FOAvip English Wikipedia <ref>{{Cite pmid|27717665}}</ref> ILC2 Suppression by Regulatory T Cells Attenuates Airway Hyperreactivity and Requires ICOS:ICOS-Ligand Interaction #MMPMID27717665 Rigas D; Lewis G; Aron JL; Wang B; Banie H; Sankaranarayanan I; Galle-Treger L; Maazi H; Lo R; Freeman GJ; Sharpe AH; Soroosh P; Akbari O J Allergy Clin Immunol 2017[May]; 139 (5): 1468-1477.e2 PMID27717665show ga Background: Atopic diseases including asthma exacerbate type 2 immune responses and involve a number of immune cell types, including regulatory T cells (Tregs) and the emerging group 2 innate lymphoid cells (ILC2s). While ILC2s are potent producers of type 2 cytokines, the regulation of ILC2 activation and function is not well understood. Objective: In the present study, we evaluate for the first time how Tregs interact with pulmonary ILC2s and control their function. Methods: ILC2s and Tregs were evaluated using in vitro suppression assays, cell-contact assays, and gene expression panels. Also, human ILC2s and Tregs were adoptively transferred into NOD SCID gamma-C deficient (NSG) mice, which were given isotype or anti-ICOS-L antibodies, then challenged with IL-33 and assessed for AHR. Results: We show that induced Tregs (iTregs), but not natural Tregs (nTregs), effectively suppress the production of ILC2-driven, pro-inflammatory cytokines IL-5 and IL-13, both in vitro and in vivo. Mechanistically, our data reveal the necessity of Inducible T cell Costimulator (ICOS):ICOS-Ligand cell contact for Treg-mediated ILC2 suppression, alongside suppressive cytokines TGF-? and IL-10. Using a translational approach, we then demonstrate that human iTregs suppress syngeneic human ILC2s via ICOS-L to control airway inflammation in a humanized ILC2 mouse model. Conclusion: These findings suggest that peripheral expansion of induced Tregs may serve as a promising therapeutic target against ILC2-dependent asthma. äILC2 Suppression by Regulatory T Cells Attenuates Airway Hyperreactivi(epmc).pdf DeepDyve Pubget Overpricing