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10.1681/ASN.2015020203 http://scihub22266oqcxt.onion/10.1681/ASN.2015020203 C4926966!4926966!26534920     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       J+Am+Soc+Nephrol 2016 ; 27 (7): 1933-42 Nephropedia Template TP {{tp|p=26534920|t=2016. CXCR3+ Regulatory T Cells Control TH1 Responses in Crescentic GN |pdf=|usr=}}{{26534920}} gab.com Text CXCR3+ Regulatory T Cells Control TH1 Responses in Crescentic GN JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=26534920 #FOAvip Chemokines and chemokine receptors are implicated in regulatory T cell (Treg) trafficking to sites of inflammation and suppression of excessive immune responses in inflammatory and autoimmune diseases; however, the specific requirements for Treg migration into the inflamed organs and the positioning of these cells within the tissue are incompletely understood. Here, we report that Tregs expressing the TH1?associated chemokine receptor CXCR3 are enriched in the kidneys of patients with ANCA?associated crescentic GN and colocalize with CXCR3+ effector T cells. To investigate the functional role of CXCR3+ Tregs, we generated mice that lack CXCR3 in Tregs specifically (Foxp3eGFP-Cre × Cxcr3fl/fl) and induced experimental crescentic GN. Treg-specific deletion of CXCR3 resulted in reduced Treg recruitment to the kidney and an overwhelming TH1 immune response, with an aggravated course of the nephritis that was reversible on anti-IFN? treatment. Together, these findings show that a subset of Tregs expresses CXCR3 and thereby, acquires trafficking properties of pathogenic CXCR3+ TH1 cells, allowing Treg localization and control of excessive TH1 responses at sites of inflammation. Twit Text FOAVip CXCR3+ Regulatory T Cells Control TH1 Responses in Crescentic GN ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=26534920 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26534920 #FOAvip English Wikipedia <ref>{{Cite pmid|26534920}}</ref> CXCR3+ Regulatory T Cells Control TH1 Responses in Crescentic GN #MMPMID26534920 Paust HJ; Riedel JH; Krebs CF; Turner JE; Brix SR; Krohn S; Velden J; Wiech T; Kaffke A; Peters A; Bennstein SB; Kapffer S; Meyer-Schwesinger C; Wegscheid C; Tiegs G; Thaiss F; Mittrücker HW; Steinmetz OM; Stahl RA; Panzer U J Am Soc Nephrol 2016[Jul]; 27 (7): 1933-42 PMID26534920show ga Chemokines and chemokine receptors are implicated in regulatory T cell (Treg) trafficking to sites of inflammation and suppression of excessive immune responses in inflammatory and autoimmune diseases; however, the specific requirements for Treg migration into the inflamed organs and the positioning of these cells within the tissue are incompletely understood. Here, we report that Tregs expressing the TH1?associated chemokine receptor CXCR3 are enriched in the kidneys of patients with ANCA?associated crescentic GN and colocalize with CXCR3+ effector T cells. To investigate the functional role of CXCR3+ Tregs, we generated mice that lack CXCR3 in Tregs specifically (Foxp3eGFP-Cre × Cxcr3fl/fl) and induced experimental crescentic GN. Treg-specific deletion of CXCR3 resulted in reduced Treg recruitment to the kidney and an overwhelming TH1 immune response, with an aggravated course of the nephritis that was reversible on anti-IFN? treatment. Together, these findings show that a subset of Tregs expresses CXCR3 and thereby, acquires trafficking properties of pathogenic CXCR3+ TH1 cells, allowing Treg localization and control of excessive TH1 responses at sites of inflammation. äCXCR3+ Regulatory T Cells Control TH1 Responses in Crescentic GN (epmc).pdf DeepDyve Pubget Overpricing