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10.1152/ajprenal.00462.2016 http://scihub22266oqcxt.onion/10.1152/ajprenal.00462.2016 C5374313!5374313 !27852609     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27852609 &cmd=llinks): Failed to open stream: HTTP request failed! 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IL-17 mediates neutrophil infiltration and renal fibrosis following recovery from ischemia reperfusion: compensatory role of natural killer cells in athymic rats |pdf=|usr=}}{{27852609 }} gab.com Text IL-17 mediates neutrophil infiltration and renal fibrosis following recovery from ischemia reperfusion: compensatory role of natural killer cells in athymic rats JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27852609 #FOAvip T cells have been implicated in the pathogenesis of acute kidney injury (AKI) and its progression to chronic kidney disease (CKD). Previous studies suggest that Th17 cells participate during the AKI-to-CKD transition, and inhibition of T cell activity by mycophenolate mofetil (MMF) or losartan attenuates the development of fibrosis following AKI. We hypothesized that T cell-deficient rats may have reduced levels of IL-17 cytokine leading to decreased fibrosis following AKI. Renal ischemis-reperfusion (I/R) was performed on T cell-deficient athymic rats (Foxn1(rnu-/rnu-)) and control euthymic rats (Foxn1(rnu-/+)), and CKD progression was hastened by unilateral nephrectomy at day 33 and subsequent exposure to 4.0% sodium diet. Renal fibrosis developed in euthymic rats and was reduced by MMF treatment. Athymic rats exhibited a similar degree of fibrosis, but this was unaffected by MMF treatment. FACS analysis demonstrated that the number of IL-17(+) cells was similar between postischemic athymic vs. euthymic rats. The source of IL-17 production in euthymic rats was predominately from conventional T cells (CD3(+)/CD161(-)). In the absence of conventional T cells in athymic rats, a compensatory pathway involving natural killer cells (CD3(-)/CD161(+)) was the primary source of IL-17. Blockade of IL-17 activity using IL-17Rc receptor significantly decreased fibrosis and neutrophil recruitment in both euthymic and athymic rats compared with vehicle-treated controls. Taken together, these data suggest that IL-17 secretion participates in the pathogenesis of AKI-induced fibrosis possibly via the recruitment of neutrophils and that the source of IL-17 may be from either conventional T cells or NK cells. Twit Text FOAVip IL-17 mediates neutrophil infiltration and renal fibrosis following recovery from ischemia reperfusion: compensatory role of natural killer cells in athymic rats ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27852609 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27852609 #FOAvip English Wikipedia <ref>{{Cite pmid|27852609 }}</ref> IL-17 mediates neutrophil infiltration and renal fibrosis following recovery from ischemia reperfusion: compensatory role of natural killer cells in athymic rats #MMPMID27852609 Mehrotra P ; Collett JA ; McKinney SD ; Stevens J ; Ivancic CM ; Basile DP Am J Physiol Renal Physiol 2017[Mar]; 312 (3 ): F385-F397 PMID27852609 show ga T cells have been implicated in the pathogenesis of acute kidney injury (AKI) and its progression to chronic kidney disease (CKD). Previous studies suggest that Th17 cells participate during the AKI-to-CKD transition, and inhibition of T cell activity by mycophenolate mofetil (MMF) or losartan attenuates the development of fibrosis following AKI. We hypothesized that T cell-deficient rats may have reduced levels of IL-17 cytokine leading to decreased fibrosis following AKI. Renal ischemis-reperfusion (I/R) was performed on T cell-deficient athymic rats (Foxn1(rnu-/rnu-)) and control euthymic rats (Foxn1(rnu-/+)), and CKD progression was hastened by unilateral nephrectomy at day 33 and subsequent exposure to 4.0% sodium diet. Renal fibrosis developed in euthymic rats and was reduced by MMF treatment. Athymic rats exhibited a similar degree of fibrosis, but this was unaffected by MMF treatment. FACS analysis demonstrated that the number of IL-17(+) cells was similar between postischemic athymic vs. euthymic rats. The source of IL-17 production in euthymic rats was predominately from conventional T cells (CD3(+)/CD161(-)). In the absence of conventional T cells in athymic rats, a compensatory pathway involving natural killer cells (CD3(-)/CD161(+)) was the primary source of IL-17. Blockade of IL-17 activity using IL-17Rc receptor significantly decreased fibrosis and neutrophil recruitment in both euthymic and athymic rats compared with vehicle-treated controls. Taken together, these data suggest that IL-17 secretion participates in the pathogenesis of AKI-induced fibrosis possibly via the recruitment of neutrophils and that the source of IL-17 may be from either conventional T cells or NK cells. |*Neutrophil Infiltration [MESH] |Acute Kidney Injury/genetics/*immunology/metabolism/pathology [MESH] |Animals [MESH] |Disease Models, Animal [MESH] |Disease Progression [MESH] |Fibrosis [MESH] |Forkhead Transcription Factors/genetics [MESH] |Genotype [MESH] |Interleukin-17/*immunology/metabolism [MESH] |Kidney/*immunology/metabolism/pathology [MESH] |Killer Cells, Natural/*immunology/metabolism [MESH] |Lymphocyte Activation [MESH] |Male [MESH] |Neutrophils/*immunology/metabolism [MESH] |Phenotype [MESH] |Rats, Nude [MESH] |Rats, Transgenic [MESH] |Renal Insufficiency, Chronic/genetics/*immunology/metabolism/pathology [MESH] |Reperfusion Injury/genetics/*immunology/metabolism/pathology [MESH] |Signal Transduction [MESH]IL-17 mediates neutrophil infiltration and renal fibrosis following re(epmc).pdf DeepDyve Pubget Overpricing