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10.1172/jci.insight.89530 http://scihub22266oqcxt.onion/10.1172/jci.insight.89530 C5333967!5333967!28289705     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28289705&cmd=llinks): Failed to open stream: HTTP request failed! 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ALS patients? regulatory T lymphocytes are dysfunctional, and correlate with disease progression rate and severity |pdf=|usr=}}{{28289705}} gab.com Text ALS patients regulatory T lymphocytes are dysfunctional, and correlate with disease progression rate and severity JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=28289705 #FOAvip Neuroinflammation is a pathological hallmark of ALS in both transgenic rodent models and patients, and is characterized by proinflammatory T lymphocytes and activated macrophages/microglia. In ALS mouse models, decreased regulatory T lymphocytes (Tregs) exacerbate the neuroinflammatory process, leading to accelerated motoneuron death and shortened survival; passive transfer of Tregs suppresses the neuroinflammation and prolongs survival. Treg numbers and FOXP3 expression are also decreased in rapidly progressing ALS patients. A key question is whether the marked neuroinflammation in ALS can be attributed to the impaired suppressive function of ALS Tregs in addition to their decreased numbers. To address this question, T lymphocyte proliferation assays were performed. Compared with control Tregs, ALS Tregs were less effective in suppressing responder T lymphocyte proliferation. Although both slowly and rapidly progressing ALS patients had dysfunctional Tregs, the greater the clinically assessed disease burden or the more rapidly progressing the patient, the greater the Treg dysfunction. Epigenetically, the percentage methylation of the Treg-specific demethylated region was greater in ALS Tregs. After in vitro expansion, ALS Tregs regained suppressive abilities to the levels of control Tregs, suggesting that autologous passive transfer of expanded Tregs might offer a novel cellular therapy to slow disease progression. Twit Text FOAVip ALS patients regulatory T lymphocytes are dysfunctional, and correlate with disease progression rate and severity ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=28289705 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28289705 #FOAvip English Wikipedia <ref>{{Cite pmid|28289705}}</ref> ALS patients? regulatory T lymphocytes are dysfunctional, and correlate with disease progression rate and severity #MMPMID28289705 Beers DR; Zhao W; Wang J; Zhang X; Wen S; Neal D; Thonhoff JR; Alsuliman AS; Shpall EJ; Rezvani K; Appel SH JCI Insight ä[]; 2 (5): ä PMID28289705show ga Neuroinflammation is a pathological hallmark of ALS in both transgenic rodent models and patients, and is characterized by proinflammatory T lymphocytes and activated macrophages/microglia. In ALS mouse models, decreased regulatory T lymphocytes (Tregs) exacerbate the neuroinflammatory process, leading to accelerated motoneuron death and shortened survival; passive transfer of Tregs suppresses the neuroinflammation and prolongs survival. Treg numbers and FOXP3 expression are also decreased in rapidly progressing ALS patients. A key question is whether the marked neuroinflammation in ALS can be attributed to the impaired suppressive function of ALS Tregs in addition to their decreased numbers. To address this question, T lymphocyte proliferation assays were performed. Compared with control Tregs, ALS Tregs were less effective in suppressing responder T lymphocyte proliferation. Although both slowly and rapidly progressing ALS patients had dysfunctional Tregs, the greater the clinically assessed disease burden or the more rapidly progressing the patient, the greater the Treg dysfunction. Epigenetically, the percentage methylation of the Treg-specific demethylated region was greater in ALS Tregs. After in vitro expansion, ALS Tregs regained suppressive abilities to the levels of control Tregs, suggesting that autologous passive transfer of expanded Tregs might offer a novel cellular therapy to slow disease progression. äALS patients? regulatory T lymphocytes are dysfunctional, and correlat(epmc).pdf DeepDyve Pubget Overpricing