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10.1111/cei.12605 http://scihub22266oqcxt.onion/10.1111/cei.12605 C4449765!4449765!25683099     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Clin+Exp+Immunol 2015 ; 180 (3): 361-70 Nephropedia Template TP {{tp|p=25683099|t=2015. The complex pathophysiology of acquired aplastic anaemia |pdf=|usr=}}{{25683099}} gab.com Text The complex pathophysiology of acquired aplastic anaemia JO: Clin Exp Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25683099 #FOAvip Immune-mediated destruction of haematopoietic stem/progenitor cells (HSPCs) plays a central role in the pathophysiology of acquired aplastic anaemia (aAA). Dysregulated CD8+ cytotoxic T cells, CD4+ T cells including T helper type 1 (Th1), Th2, regulatory T cells and Th17 cells, natural killer (NK) cells and NK T cells, along with the abnormal production of cytokines including interferon (IFN)-?, tumour necrosis factor (TNF)-? and transforming growth factor (TGF)-?, induce apoptosis of HSPCs, constituting a consistent and defining feature of severe aAA. Alterations in the polymorphisms of TGF-?, IFN-? and TNF-? genes, as well as certain human leucocyte antigen (HLA) alleles, may account for the propensity to immune-mediated killing of HSPCs and/or ineffective haematopoiesis. Although the inciting autoantigens remain elusive, autoantibodies are often detected in the serum. In addition, recent studies provide genetic and molecular evidence that intrinsic and/or secondary deficits in HSPCs and bone marrow mesenchymal stem cells may underlie the development of bone marrow failure. Twit Text FOAVip The complex pathophysiology of acquired aplastic anaemia ????Clin Exp Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25683099 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25683099 #FOAvip English Wikipedia <ref>{{Cite pmid|25683099}}</ref> The complex pathophysiology of acquired aplastic anaemia #MMPMID25683099 Zeng Y; Katsanis E Clin Exp Immunol 2015[Jun]; 180 (3): 361-70 PMID25683099show ga Immune-mediated destruction of haematopoietic stem/progenitor cells (HSPCs) plays a central role in the pathophysiology of acquired aplastic anaemia (aAA). Dysregulated CD8+ cytotoxic T cells, CD4+ T cells including T helper type 1 (Th1), Th2, regulatory T cells and Th17 cells, natural killer (NK) cells and NK T cells, along with the abnormal production of cytokines including interferon (IFN)-?, tumour necrosis factor (TNF)-? and transforming growth factor (TGF)-?, induce apoptosis of HSPCs, constituting a consistent and defining feature of severe aAA. Alterations in the polymorphisms of TGF-?, IFN-? and TNF-? genes, as well as certain human leucocyte antigen (HLA) alleles, may account for the propensity to immune-mediated killing of HSPCs and/or ineffective haematopoiesis. Although the inciting autoantigens remain elusive, autoantibodies are often detected in the serum. In addition, recent studies provide genetic and molecular evidence that intrinsic and/or secondary deficits in HSPCs and bone marrow mesenchymal stem cells may underlie the development of bone marrow failure. äThe complex pathophysiology of acquired aplastic anaemia (epmc).pdf DeepDyve Pubget Overpricing