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10.1073/pnas.1418549112 http://scihub22266oqcxt.onion/10.1073/pnas.1418549112 C4386370!4386370 !25829541     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25829541 &cmd=llinks): Failed to open stream: HTTP request failed! 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T-bet- and STAT4-dependent IL-33 receptor expression directly promotes antiviral Th1 cell responses |pdf=|usr=}}{{25829541 }} gab.com Text T-bet- and STAT4-dependent IL-33 receptor expression directly promotes antiviral Th1 cell responses JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=25829541 #FOAvip During infection, the release of damage-associated molecular patterns, so-called "alarmins," orchestrates the immune response. The alarmin IL-33 plays a role in a wide range of pathologies. Upon release, IL-33 signals through its receptor ST2, which reportedly is expressed only on CD4(+) T cells of the Th2 and regulatory subsets. Here we show that Th1 effector cells also express ST2 upon differentiation in vitro and in vivo during lymphocytic choriomeningitis virus (LCMV) infection. The expression of ST2 on Th1 cells was transient, in contrast to constitutive ST2 expression on Th2 cells, and marked highly activated effector cells. ST2 expression on virus-specific Th1 cells depended on the Th1-associated transcription factors T-bet and STAT4. ST2 deficiency resulted in a T-cell-intrinsic impairment of LCMV-specific Th1 effector responses in both mixed bone marrow-chimeric mice and adoptive cell transfer experiments. ST2-deficient virus-specific CD4(+) T cells showed impaired expansion, Th1 effector differentiation, and antiviral cytokine production. Consequently, these cells mediated little virus-induced immunopathology. Thus, IL-33 acts as a critical and direct cofactor to drive antiviral Th1 effector cell activation, with implications for vaccination strategies and immunotherapeutic approaches. Twit Text FOAVip T-bet- and STAT4-dependent IL-33 receptor expression directly promotes antiviral Th1 cell responses ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=25829541 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25829541 #FOAvip English Wikipedia <ref>{{Cite pmid|25829541 }}</ref> T-bet- and STAT4-dependent IL-33 receptor expression directly promotes antiviral Th1 cell responses #MMPMID25829541 Baumann C ; Bonilla WV ; Fröhlich A ; Helmstetter C ; Peine M ; Hegazy AN ; Pinschewer DD ; Löhning M Proc Natl Acad Sci U S A 2015[Mar]; 112 (13 ): 4056-61 PMID25829541 show ga During infection, the release of damage-associated molecular patterns, so-called "alarmins," orchestrates the immune response. The alarmin IL-33 plays a role in a wide range of pathologies. Upon release, IL-33 signals through its receptor ST2, which reportedly is expressed only on CD4(+) T cells of the Th2 and regulatory subsets. Here we show that Th1 effector cells also express ST2 upon differentiation in vitro and in vivo during lymphocytic choriomeningitis virus (LCMV) infection. The expression of ST2 on Th1 cells was transient, in contrast to constitutive ST2 expression on Th2 cells, and marked highly activated effector cells. ST2 expression on virus-specific Th1 cells depended on the Th1-associated transcription factors T-bet and STAT4. ST2 deficiency resulted in a T-cell-intrinsic impairment of LCMV-specific Th1 effector responses in both mixed bone marrow-chimeric mice and adoptive cell transfer experiments. ST2-deficient virus-specific CD4(+) T cells showed impaired expansion, Th1 effector differentiation, and antiviral cytokine production. Consequently, these cells mediated little virus-induced immunopathology. Thus, IL-33 acts as a critical and direct cofactor to drive antiviral Th1 effector cell activation, with implications for vaccination strategies and immunotherapeutic approaches. |*Gene Expression Regulation [MESH] |Animals [MESH] |Arenaviridae Infections/*immunology [MESH] |CD8-Positive T-Lymphocytes/cytology/immunology [MESH] |Cell Differentiation [MESH] |Cell Separation [MESH] |Flow Cytometry [MESH] |Gene Expression Profiling [MESH] |Hyaluronan Receptors/metabolism [MESH] |Interferon-gamma/metabolism [MESH] |Interleukin-33 [MESH] |Interleukins/*immunology [MESH] |L-Selectin/metabolism [MESH] |Lymphocytic choriomeningitis virus [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |STAT4 Transcription Factor/*metabolism [MESH] |T-Box Domain Proteins/*metabolism [MESH] |T-Lymphocytes/cytology [MESH] |T-bet Transcription Factor [MESH]T-bet- and STAT4-dependent IL-33 receptor expression directly promotes(epmc).pdf DeepDyve Pubget Overpricing