NDLI: Chromatin decondensation and T cell hyperresponsiveness in diabetes-associated hyperglycemia.

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Chromatin decondensation and T cell hyperresponsiveness in diabetes-associated hyperglycemia.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lee, Jinhee Vallerskog, Therese Martinez, Nuria Martens, Gregory W. Nunes-Alves, Claudio Kornfeld, Hardy West, Kim Behar, Samuel M.
Description	Author Affiliation: Martinez N ( Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655); Vallerskog T ( Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655); West K ( Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655); Nunes-Alves C ( Department of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, MA 01655.); Lee J ( Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655); Martens GW ( Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655); Behar SM ( Department of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, MA 01655.); Kornfeld H ( Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655)
Abstract	Diabetes is linked to increased inflammation and susceptibility to certain infectious diseases including tuberculosis (TB). We previously reported that aerosol TB in mice with chronic (≥ 12 wk) hyperglycemia features increased bacterial load, overproduction of several cytokines, and increased immune pathology compared with normoglycemic controls. A similar phenotype exists in human patients with diabetes with TB. The mechanisms of increased T cell activation in diabetes are unknown. In the current study, we tested the hypothesis that hyperglycemia modifies the intrinsic responsiveness of naive T cells to TCR stimulation. Purified T cells from chronically hyperglycemic (HG) mice produced higher levels of Th1, Th2, and Th17 cytokines and proliferated more than T cells from normoglycemic controls after anti-CD3e or Ag stimulation. In this way, naive T cells from HG mice resembled Ag-experienced cells, although CD44 expression was not increased. Chromatin decondensation, another characteristic of Ag-experienced T cells, was increased in naive T cells from HG mice. That phenotype depended on expression of the receptor for advanced glycation end products and could be reversed by inhibiting p38 MAPK. Chromatin decondensation and hyperresponsiveness to TCR stimulation persisted following transfer of T cells from HG mice into normoglycemic mice. We propose that chronic hyperglycemia causes receptor for advanced glycation end products-mediated epigenetic modification of naive T cells leading to p38 MAPK-dependent chromatin decondensation. This preactivation state facilitates transcription factor access to DNA, increasing cytokine production and proliferation following TCR stimulation. This mechanism may contribute to pathological inflammation associated with diabetes and might offer a novel therapeutic target.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1401125
Journal	The Journal of Immunology
Issue Number	9
Volume Number	193
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Chromatin Genetics Diabetes Mellitus Immunology Hyperglycemia T-lymphocyte Subsets Metabolism Advanced Glycosylation End Product-specific Receptor Animals Antigen-presenting Cells Bone Marrow Cells Cytokines Biosynthesis Disease Models, Animal Gene Expression Hematopoietic Stem Cells Immunophenotyping Lymphocyte Activation Map Kinase Signaling System Mice Mice, Knockout Phenotype Receptors, Immunologic Thymus Gland Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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