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10.1111/imr.12549 http://scihub22266oqcxt.onion/10.1111/imr.12549 C5492958!5492958 !28658543     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28658543 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Immunol+Rev 2017 ; 278 (1 ): 20-40 Nephropedia Template TP {{tp|p=28658543 |t=2017. Modeling T(H) 2 responses and airway inflammation to understand fundamental mechanisms regulating the pathogenesis of asthma |pdf=|usr=}}{{28658543 }} gab.com Text Modeling T(H) 2 responses and airway inflammation to understand fundamental mechanisms regulating the pathogenesis of asthma JO: Immunol Rev http://www.kidney.de/pget.php?&tw=1&pmid=28658543 #FOAvip In this review, we highlight experiments conducted in our laboratories that have elucidated functional roles for CD4(+) T-helper type-2 lymphocytes (T(H) 2 cells), their associated cytokines, and eosinophils in the regulation of hallmark features of allergic asthma. Notably, we consider the complexity of type-2 responses and studies that have explored integrated signaling among classical T(H) 2 cytokines (IL-4, IL-5, and IL-13), which together with CCL11 (eotaxin-1) regulate critical aspects of eosinophil recruitment, allergic inflammation, and airway hyper-responsiveness (AHR). Among our most important findings, we have provided evidence that the initiation of T(H) 2 responses is regulated by airway epithelial cell-derived factors, including TRAIL and MID1, which promote T(H) 2 cell development via STAT6-dependent pathways. Further, we highlight studies demonstrating that microRNAs are key regulators of allergic inflammation and potential targets for anti-inflammatory therapy. On the background of T(H) 2 inflammation, we have demonstrated that innate immune cells (notably, airway macrophages) play essential roles in the generation of steroid-resistant inflammation and AHR secondary to allergen- and pathogen-induced exacerbations. Our work clearly indicates that understanding the diversity and spatiotemporal role of the inflammatory response and its interactions with resident airway cells is critical to advancing knowledge on asthma pathogenesis and the development of new therapeutic approaches. Twit Text FOAVip Modeling T(H) 2 responses and airway inflammation to understand fundamental mechanisms regulating the pathogenesis of asthma ????Immunol Rev http://www.kidney.de/pget.php?&tw=1&pmid=28658543 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28658543 #FOAvip English Wikipedia <ref>{{Cite pmid|28658543 }}</ref> Modeling T(H) 2 responses and airway inflammation to understand fundamental mechanisms regulating the pathogenesis of asthma #MMPMID28658543 Foster PS ; Maltby S ; Rosenberg HF ; Tay HL ; Hogan SP ; Collison AM ; Yang M ; Kaiko GE ; Hansbro PM ; Kumar RK ; Mattes J Immunol Rev 2017[Jul]; 278 (1 ): 20-40 PMID28658543 show ga In this review, we highlight experiments conducted in our laboratories that have elucidated functional roles for CD4(+) T-helper type-2 lymphocytes (T(H) 2 cells), their associated cytokines, and eosinophils in the regulation of hallmark features of allergic asthma. Notably, we consider the complexity of type-2 responses and studies that have explored integrated signaling among classical T(H) 2 cytokines (IL-4, IL-5, and IL-13), which together with CCL11 (eotaxin-1) regulate critical aspects of eosinophil recruitment, allergic inflammation, and airway hyper-responsiveness (AHR). Among our most important findings, we have provided evidence that the initiation of T(H) 2 responses is regulated by airway epithelial cell-derived factors, including TRAIL and MID1, which promote T(H) 2 cell development via STAT6-dependent pathways. Further, we highlight studies demonstrating that microRNAs are key regulators of allergic inflammation and potential targets for anti-inflammatory therapy. On the background of T(H) 2 inflammation, we have demonstrated that innate immune cells (notably, airway macrophages) play essential roles in the generation of steroid-resistant inflammation and AHR secondary to allergen- and pathogen-induced exacerbations. Our work clearly indicates that understanding the diversity and spatiotemporal role of the inflammatory response and its interactions with resident airway cells is critical to advancing knowledge on asthma pathogenesis and the development of new therapeutic approaches. |*Models, Biological [MESH] |Animals [MESH] |Anti-Asthmatic Agents/pharmacology/therapeutic use [MESH] |Antibodies, Anti-Idiotypic/pharmacology/therapeutic use [MESH] |Asthma/drug therapy/*etiology/*metabolism/pathology [MESH] |Cell Communication [MESH] |Chemokine CCL11/metabolism [MESH] |Cytokines/metabolism/pharmacology/therapeutic use [MESH] |Disease Susceptibility [MESH] |Drug Resistance [MESH] |Humans [MESH] |Immune System/cytology/immunology/metabolism [MESH] |Immunoglobulin E/immunology [MESH] |Immunomodulation [MESH] |MicroRNAs/genetics [MESH] |Respiratory Hypersensitivity/etiology/metabolism/pathology [MESH] |Signal Transduction [MESH] |T-Lymphocyte Subsets/immunology/metabolism [MESH]Modeling T(H) 2 responses and airway inflammation to understand fundam(epmc).pdf DeepDyve Pubget Overpricing