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10.1038/s41590-021-01080-3 http://scihub22266oqcxt.onion/10.1038/s41590-021-01080-3 34764490!7612139!34764490     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       Nat+Immunol 2022 ; 23 (1): 62-74 Nephropedia Template TP {{tp|p=34764490|t=2022. Autocrine vitamin D signaling switches off pro-inflammatory programs of T(H)1 cells |pdf=|usr=}}{{34764490}} gab.com Text Autocrine vitamin D signaling switches off pro-inflammatory programs of T(H)1 cells JO: Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34764490 #FOAvip The molecular mechanisms governing orderly shutdown and retraction of CD4(+) type 1 helper T (T(H)1) cell responses remain poorly understood. Here we show that complement triggers contraction of T(H)1 responses by inducing intrinsic expression of the vitamin D (VitD) receptor and the VitD-activating enzyme CYP27B1, permitting T cells to both activate and respond to VitD. VitD then initiated the transition from pro-inflammatory interferon-gamma(+) T(H)1 cells to suppressive interleukin-10(+) cells. This process was primed by dynamic changes in the epigenetic landscape of CD4(+) T cells, generating super-enhancers and recruiting several transcription factors, notably c-JUN, STAT3 and BACH2, which together with VitD receptor shaped the transcriptional response to VitD. Accordingly, VitD did not induce interleukin-10 expression in cells with dysfunctional BACH2 or STAT3. Bronchoalveolar lavage fluid CD4(+) T cells of patients with COVID-19 were T(H)1-skewed and showed de-repression of genes downregulated by VitD, from either lack of substrate (VitD deficiency) and/or abnormal regulation of this system. Twit Text FOAVip Autocrine vitamin D signaling switches off pro-inflammatory programs of T(H)1 cells ????Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34764490 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34764490 #FOAvip English Wikipedia <ref>{{Cite pmid|34764490}}</ref> Autocrine vitamin D signaling switches off pro-inflammatory programs of T(H)1 cells #MMPMID34764490 Chauss D; Freiwald T; McGregor R; Yan B; Wang L; Nova-Lamperti E; Kumar D; Zhang Z; Teague H; West EE; Vannella KM; Ramos-Benitez MJ; Bibby J; Kelly A; Malik A; Freeman AF; Schwartz DM; Portilla D; Chertow DS; John S; Lavender P; Kemper C; Lombardi G; Mehta NN; Cooper N; Lionakis MS; Laurence A; Kazemian M; Afzali B Nat Immunol 2022[Jan]; 23 (1): 62-74 PMID34764490show ga The molecular mechanisms governing orderly shutdown and retraction of CD4(+) type 1 helper T (T(H)1) cell responses remain poorly understood. Here we show that complement triggers contraction of T(H)1 responses by inducing intrinsic expression of the vitamin D (VitD) receptor and the VitD-activating enzyme CYP27B1, permitting T cells to both activate and respond to VitD. VitD then initiated the transition from pro-inflammatory interferon-gamma(+) T(H)1 cells to suppressive interleukin-10(+) cells. This process was primed by dynamic changes in the epigenetic landscape of CD4(+) T cells, generating super-enhancers and recruiting several transcription factors, notably c-JUN, STAT3 and BACH2, which together with VitD receptor shaped the transcriptional response to VitD. Accordingly, VitD did not induce interleukin-10 expression in cells with dysfunctional BACH2 or STAT3. Bronchoalveolar lavage fluid CD4(+) T cells of patients with COVID-19 were T(H)1-skewed and showed de-repression of genes downregulated by VitD, from either lack of substrate (VitD deficiency) and/or abnormal regulation of this system. |25-Hydroxyvitamin D3 1-alpha-Hydroxylase/metabolism[MESH] |Basic-Leucine Zipper Transcription Factors/metabolism[MESH] |Bronchoalveolar Lavage Fluid/cytology[MESH] |COVID-19/immunology/pathology[MESH] |Complement C3a/immunology[MESH] |Complement C3b/immunology[MESH] |Humans[MESH] |Interferon-gamma/*immunology[MESH] |Interleukin-10/*immunology[MESH] |JNK Mitogen-Activated Protein Kinases/metabolism[MESH] |Lymphocyte Activation/immunology[MESH] |Receptors, Calcitriol/metabolism[MESH] |Respiratory Distress Syndrome/immunology/pathology/virology[MESH] |SARS-CoV-2/*immunology[MESH] |STAT3 Transcription Factor/metabolism[MESH] |Signal Transduction/immunology[MESH] |Th1 Cells/*immunology[MESH] |Transcription, Genetic/genetics[MESH]Autocrine vitamin D signaling switches off pro-inflammatory programs o(epmc).pdf DeepDyve Pubget Overpricing