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10.4049/jimmunol.1302062 http://scihub22266oqcxt.onion/10.4049/jimmunol.1302062 C3984038!3984038 !24616478     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24616478 &cmd=llinks): Failed to open stream: HTTP request failed! 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Metabolic reprogramming is required for antibody production that is suppressed in anergic but exaggerated in chronically BAFF-exposed B cells |pdf=|usr=}}{{24616478 }} gab.com Text Metabolic reprogramming is required for antibody production that is suppressed in anergic but exaggerated in chronically BAFF-exposed B cells JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24616478 #FOAvip B cell activation leads to proliferation and Ab production that can protect from pathogens or promote autoimmunity. Regulation of cell metabolism is essential to support the demands of lymphocyte growth and effector function and may regulate tolerance. In this study, we tested the regulation and role of glucose uptake and metabolism in the proliferation and Ab production of control, anergic, and autoimmune-prone B cells. Control B cells had a balanced increase in lactate production and oxygen consumption following activation, with proportionally increased glucose transporter Glut1 expression and mitochondrial mass upon either LPS or BCR stimulation. This contrasted with metabolic reprogramming of T cells, which had lower glycolytic flux when resting but disproportionately increased this pathway upon activation. Importantly, tolerance greatly affected B cell metabolic reprogramming. Anergic B cells remained metabolically quiescent, with only a modest increase in glycolysis and oxygen consumption with LPS stimulation. B cells chronically stimulated with elevated BAFF, however, rapidly increased glycolysis and Ab production upon stimulation. Induction of glycolysis was critical for Ab production, as glycolytic inhibition with the pyruvate dehydrogenase kinase inhibitor dichloroacetate sharply suppressed B cell proliferation and Ab secretion in vitro and in vivo. Furthermore, B cell-specific deletion of Glut1 led to reduced B cell numbers and impaired Ab production in vivo. Together, these data show that activated B cells require Glut1-dependent metabolic reprogramming to support proliferation and Ab production that is distinct from T cells and that this glycolytic reprogramming is regulated in tolerance. Twit Text FOAVip Metabolic reprogramming is required for antibody production that is suppressed in anergic but exaggerated in chronically BAFF-exposed B cells ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24616478 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24616478 #FOAvip English Wikipedia <ref>{{Cite pmid|24616478 }}</ref> Metabolic reprogramming is required for antibody production that is suppressed in anergic but exaggerated in chronically BAFF-exposed B cells #MMPMID24616478 Caro-Maldonado A ; Wang R ; Nichols AG ; Kuraoka M ; Milasta S ; Sun LD ; Gavin AL ; Abel ED ; Kelsoe G ; Green DR ; Rathmell JC J Immunol 2014[Apr]; 192 (8 ): 3626-36 PMID24616478 show ga B cell activation leads to proliferation and Ab production that can protect from pathogens or promote autoimmunity. Regulation of cell metabolism is essential to support the demands of lymphocyte growth and effector function and may regulate tolerance. In this study, we tested the regulation and role of glucose uptake and metabolism in the proliferation and Ab production of control, anergic, and autoimmune-prone B cells. Control B cells had a balanced increase in lactate production and oxygen consumption following activation, with proportionally increased glucose transporter Glut1 expression and mitochondrial mass upon either LPS or BCR stimulation. This contrasted with metabolic reprogramming of T cells, which had lower glycolytic flux when resting but disproportionately increased this pathway upon activation. Importantly, tolerance greatly affected B cell metabolic reprogramming. Anergic B cells remained metabolically quiescent, with only a modest increase in glycolysis and oxygen consumption with LPS stimulation. B cells chronically stimulated with elevated BAFF, however, rapidly increased glycolysis and Ab production upon stimulation. Induction of glycolysis was critical for Ab production, as glycolytic inhibition with the pyruvate dehydrogenase kinase inhibitor dichloroacetate sharply suppressed B cell proliferation and Ab secretion in vitro and in vivo. Furthermore, B cell-specific deletion of Glut1 led to reduced B cell numbers and impaired Ab production in vivo. Together, these data show that activated B cells require Glut1-dependent metabolic reprogramming to support proliferation and Ab production that is distinct from T cells and that this glycolytic reprogramming is regulated in tolerance. |*Antibody Formation [MESH] |Animals [MESH] |B-Cell Activating Factor/genetics/*metabolism [MESH] |B-Lymphocytes/*immunology/*metabolism [MESH] |Clonal Anergy/*immunology [MESH] |Dichloroacetic Acid/pharmacology [MESH] |Glucose Transporter Type 1/metabolism [MESH] |Glucose/metabolism [MESH] |Glycolysis/drug effects [MESH] |Homeostasis [MESH] |Humans [MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/metabolism [MESH] |Lymphocyte Activation/immunology [MESH] |Mice [MESH] |Mice, Transgenic [MESH] |Mitochondria/metabolism [MESH] |Protein Serine-Threonine Kinases/antagonists & inhibitors [MESH] |Proto-Oncogene Proteins c-myc/metabolism [MESH] |Pyruvate Dehydrogenase Acetyl-Transferring Kinase [MESH]Metabolic reprogramming is required for antibody production that is su(epmc).pdf DeepDyve Pubget Overpricing