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10.1053/j.gastro.2011.04.053 http://scihub22266oqcxt.onion/10.1053/j.gastro.2011.04.053 C4651012!4651012 !21679711     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=21679711 &cmd=llinks): Failed to open stream: HTTP request failed! 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Antigen-presenting cell production of IL-10 inhibits T-helper 1 and 17 cell responses and suppresses colitis in mice |pdf=|usr=}}{{21679711 }} gab.com Text Antigen-presenting cell production of IL-10 inhibits T-helper 1 and 17 cell responses and suppresses colitis in mice JO: Gastroenterology http://www.kidney.de/pget.php?&tw=1&pmid=21679711 #FOAvip BACKGROUND & AIMS: Mice that are deficient in interleukin (IL)-10 develop colitis, mediated by T-helper (Th)1 and Th17 cells, and IL-10-producing regulatory T (Treg) cells suppress colitis, implicating IL-10 in maintaining mucosal homeostasis. We assessed the relative importance of immunoregulatory IL-10 derived from T cells or from antigen presenting cells (APCs) in development of intestinal inflammation. METHODS: CD4(+) cells from germ-free (GF) or specific pathogen-free (SPF) IL-10(-/-) or wild-type mice were injected into IL-10(-/-), Rag2(-/-) mice or Rag2(-/-) mice that express IL-10. After 6-8 weeks, we evaluated inflammation, spontaneous secretion of cytokines from colonic tissue, and mRNA levels of the transcription factor T-bet and the immunoregulatory cytokine transforming growth factor (TGF)-?. CD4(+) T cells were co-cultured with bacterial lysate-pulsed APCs and assayed for cytokine production, FoxP3 expression, and TGF-?-mediated Smad signaling. RESULTS: CD4(+) cells from GF or SPF IL-10(-/-) or wild-type mice induced more severe colitis and higher levels of inflammatory cytokines in IL-10(-/-), Rag2(-/-) mice than in IL-10-replete, Rag2(-/-) mice. Co-cultures of IL-10(-/-) or wild-type CD4(+) T cells plus bacterial lysate-pulsed APCs from IL-10(-/-) mice contained more interferon (IFN)-?, IL-12/23p40, and IL-17 than co-cultures of the same T cells plus APCs from wild-type mice. CD11b(+) APCs were required for these effects. Blocking IL-10 receptors increased production of IFN-? and IL-12/23p40 whereas exogenous IL-10 suppressed these cytokines. IL-10-producing APCs induced TGF-?-mediated, retinoic acid-dependent, differentiation of FoxP3(+) Treg cells, whereas blocking the retinoic acid receptor, in vitro and in vivo, reduced proportions of FoxP3(+) Treg cells. CONCLUSIONS: IL-10 produced by APCs regulates homeostatic T-cell responses to commensal bacteria. Twit Text FOAVip Antigen-presenting cell production of IL-10 inhibits T-helper 1 and 17 cell responses and suppresses colitis in mice ????Gastroenterology http://www.kidney.de/pget.php?&tw=1&pmid=21679711 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21679711 #FOAvip English Wikipedia <ref>{{Cite pmid|21679711 }}</ref> Antigen-presenting cell production of IL-10 inhibits T-helper 1 and 17 cell responses and suppresses colitis in mice #MMPMID21679711 Liu B ; Tonkonogy SL ; Sartor RB Gastroenterology 2011[Aug]; 141 (2 ): 653-62, 662.e1-4 PMID21679711 show ga BACKGROUND & AIMS: Mice that are deficient in interleukin (IL)-10 develop colitis, mediated by T-helper (Th)1 and Th17 cells, and IL-10-producing regulatory T (Treg) cells suppress colitis, implicating IL-10 in maintaining mucosal homeostasis. We assessed the relative importance of immunoregulatory IL-10 derived from T cells or from antigen presenting cells (APCs) in development of intestinal inflammation. METHODS: CD4(+) cells from germ-free (GF) or specific pathogen-free (SPF) IL-10(-/-) or wild-type mice were injected into IL-10(-/-), Rag2(-/-) mice or Rag2(-/-) mice that express IL-10. After 6-8 weeks, we evaluated inflammation, spontaneous secretion of cytokines from colonic tissue, and mRNA levels of the transcription factor T-bet and the immunoregulatory cytokine transforming growth factor (TGF)-?. CD4(+) T cells were co-cultured with bacterial lysate-pulsed APCs and assayed for cytokine production, FoxP3 expression, and TGF-?-mediated Smad signaling. RESULTS: CD4(+) cells from GF or SPF IL-10(-/-) or wild-type mice induced more severe colitis and higher levels of inflammatory cytokines in IL-10(-/-), Rag2(-/-) mice than in IL-10-replete, Rag2(-/-) mice. Co-cultures of IL-10(-/-) or wild-type CD4(+) T cells plus bacterial lysate-pulsed APCs from IL-10(-/-) mice contained more interferon (IFN)-?, IL-12/23p40, and IL-17 than co-cultures of the same T cells plus APCs from wild-type mice. CD11b(+) APCs were required for these effects. Blocking IL-10 receptors increased production of IFN-? and IL-12/23p40 whereas exogenous IL-10 suppressed these cytokines. IL-10-producing APCs induced TGF-?-mediated, retinoic acid-dependent, differentiation of FoxP3(+) Treg cells, whereas blocking the retinoic acid receptor, in vitro and in vivo, reduced proportions of FoxP3(+) Treg cells. CONCLUSIONS: IL-10 produced by APCs regulates homeostatic T-cell responses to commensal bacteria. |*Germ-Free Life [MESH] |Adaptive Immunity [MESH] |Animals [MESH] |Antigen-Presenting Cells/drug effects/metabolism [MESH] |Antigens, Bacterial/*immunology [MESH] |CD11b Antigen/metabolism [MESH] |CD4-Positive T-Lymphocytes/*metabolism [MESH] |Cells, Cultured [MESH] |Colitis/*immunology [MESH] |DNA-Binding Proteins/deficiency/genetics [MESH] |Forkhead Transcription Factors/metabolism [MESH] |Immunity, Innate [MESH] |Interferon-gamma/metabolism [MESH] |Interleukin-10/deficiency/genetics/*immunology/*metabolism/pharmacology [MESH] |Interleukin-12/metabolism [MESH] |Interleukin-17/metabolism [MESH] |Mice [MESH] |Mice, Knockout [MESH] |RNA, Messenger/*metabolism [MESH] |Signal Transduction [MESH] |Smad Proteins [MESH] |T-Box Domain Proteins/metabolism [MESH] |T-Lymphocytes, Regulatory/cytology [MESH] |T-bet Transcription Factor [MESH] |Th1 Cells/immunology [MESH] |Th17 Cells/immunology [MESH] |Transforming Growth Factor beta/metabolism [MESH]Antigen-presenting cell production of IL-10 inhibits T-helper 1 and 17(epmc).pdf DeepDyve Pubget Overpricing