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10.4049/jimmunol.1601299 http://scihub22266oqcxt.onion/10.4049/jimmunol.1601299 C5543699!5543699!28630090     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28630090&cmd=llinks): Failed to open stream: HTTP request failed! 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T Cell Transcriptomes from Paroxysmal Nocturnal Hemoglobinuria Patients Reveal Novel Signaling Pathways |pdf=|usr=}}{{28630090}} gab.com Text T Cell Transcriptomes from Paroxysmal Nocturnal Hemoglobinuria Patients Reveal Novel Signaling Pathways JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28630090 #FOAvip Paroxysmal nocturnal hemoglobinuria (PNH) is a rare acquired disorder originating from hematopoietic stem cells (HSCs) and a life-threating disease characterized by intravascular hemolysis, bone marrow (BM) failure, and venous thrombosis. The etiology of PNH is a somatic mutation in the phosphatidylinositol glycan class A gene (PIG-A) on the X chromosome, which blocks synthesis of the glycolipid moiety and causes deficiency in glycosyl phosphatidylinositol?anchored proteins (GPI-APs). PNH is closely related to aplastic anemia, in which T cells mediate destruction of BM. In order to identify aberrant molecular mechanisms involved in immune targeting of HSCs in BM, RNA-seq was applied to examine the transcriptome of T cell subsets (CD4+ na�ve, CD4+ memory, CD8+ na�ve, and CD8+ memory) from PNH patients and healthy controls. Differentially expressed gene analysis in four different T cell subsets from PNH and healthy controls showed distinct transcriptional profiles, depending on the T cell subset. By pathway analysis, we identified novel signaling pathways in T cell subsets from PNH, including increased gene expression involved in TNFR, IGF1, NOTCH, AP1, and ATF2 pathways. Dysregulation of several candidate genes (JUN, TNFAIP3, TOB1, GIMAP4, GIMAP6, TRMT112, NR4A2, CD69, and TNFSF8) was validated by quantitative real-time RT-PCR and flow cytometry. We have demonstrated molecular signatures associated with positive and negative regulators in T cells, suggesting novel pathophysiologic mechanisms in PNH. These pathways may be targets for new strategies to modulate T cell immune responses in BM failure. Twit Text FOAVip T Cell Transcriptomes from Paroxysmal Nocturnal Hemoglobinuria Patients Reveal Novel Signaling Pathways ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28630090 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28630090 #FOAvip English Wikipedia <ref>{{Cite pmid|28630090}}</ref> T Cell Transcriptomes from Paroxysmal Nocturnal Hemoglobinuria Patients Reveal Novel Signaling Pathways #MMPMID28630090 Hosokawa K; Kajigaya S; Keyvanfar K; Qiao W; Xie Y; Townsley DM; Feng X; Young NS J Immunol 2017[Jul]; 199 (2): 477-88 PMID28630090show ga Paroxysmal nocturnal hemoglobinuria (PNH) is a rare acquired disorder originating from hematopoietic stem cells (HSCs) and a life-threating disease characterized by intravascular hemolysis, bone marrow (BM) failure, and venous thrombosis. The etiology of PNH is a somatic mutation in the phosphatidylinositol glycan class A gene (PIG-A) on the X chromosome, which blocks synthesis of the glycolipid moiety and causes deficiency in glycosyl phosphatidylinositol?anchored proteins (GPI-APs). PNH is closely related to aplastic anemia, in which T cells mediate destruction of BM. In order to identify aberrant molecular mechanisms involved in immune targeting of HSCs in BM, RNA-seq was applied to examine the transcriptome of T cell subsets (CD4+ na�ve, CD4+ memory, CD8+ na�ve, and CD8+ memory) from PNH patients and healthy controls. Differentially expressed gene analysis in four different T cell subsets from PNH and healthy controls showed distinct transcriptional profiles, depending on the T cell subset. By pathway analysis, we identified novel signaling pathways in T cell subsets from PNH, including increased gene expression involved in TNFR, IGF1, NOTCH, AP1, and ATF2 pathways. Dysregulation of several candidate genes (JUN, TNFAIP3, TOB1, GIMAP4, GIMAP6, TRMT112, NR4A2, CD69, and TNFSF8) was validated by quantitative real-time RT-PCR and flow cytometry. We have demonstrated molecular signatures associated with positive and negative regulators in T cells, suggesting novel pathophysiologic mechanisms in PNH. These pathways may be targets for new strategies to modulate T cell immune responses in BM failure. �T Cell Transcriptomes from Paroxysmal Nocturnal Hemoglobinuria Patient(epmc).pdf DeepDyve Pubget Overpricing