NDLI: Metabolic reprogramming is required for antibody production that is suppressed in anergic but exaggerated in chronically BAFF-exposed B cells.

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Metabolic reprogramming is required for antibody production that is suppressed in anergic but exaggerated in chronically BAFF-exposed B cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Milasta, Sandra Sun, Lillian D. Nichols, Amanda G. Abel, E. Dale Gavin, Amanda L. Caro-Maldonado, Alfredo Kelsoe, Garnett Kuraoka, Masayuki Green, Douglas R. Rathmell, Jeffrey C. Wang, Ruoning
Description	Author Affiliation: Caro-Maldonado A ( Department of Pharmacology and Cancer Biology, Duke University, Durham, NC 27710)
Abstract	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.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1302062
Journal	The Journal of Immunology
Issue Number	8
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-04-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antibody Formation B-cell Activating Factor Metabolism B-lymphocytes Immunology Clonal Anergy Animals Genetics Dichloroacetic Acid Pharmacology Glucose Glucose Transporter Type 1 Glycolysis Drug Effects Homeostasis Hypoxia-inducible Factor 1, Alpha Subunit Lymphocyte Activation Mice Mice, Transgenic Mitochondria Protein-serine-threonine Kinases Antagonists & Inhibitors Proto-oncogene Proteins C-myc T-lymphocytes Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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BAFF-Exposed B Cells Anergic but Exaggerated in Chronically Antibody Production That Is Suppressed in Metabolic Reprogramming Is Required for Green and

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Metabolic reprogramming is required for antibody production that is suppressed in anergic but exaggerated in chronically BAFF-exposed B cells.

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Metabolic reprogramming is required for antibody production that is suppressed in anergic but exaggerated in chronically BAFF-exposed B cells.