NDLI: Cutting Edge: Nonobese Diabetic Mice Deficient in Chromogranin A Are Protected from Autoimmune Diabetes.

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Cutting Edge: Nonobese Diabetic Mice Deficient in Chromogranin A Are Protected from Autoimmune Diabetes.

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Cutting Edge: Nonobese Diabetic Mice Deficient in Chromogranin A Are Protected from Autoimmune Diabetes.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Baker, Rocky L. Barbour, Gene Wiles, Timothy A. Delong, Thomas Haskins, Kathryn Bradley, Brenda Lindsay, Robin S. Friedman, Rachel S.
Description	Author Affiliation: Baker RL ( Department of Immunology and Microbiology, University of Colorado School of Medicine at Denver, Aurora, CO 80045); Bradley B ( Department of Immunology and Microbiology, University of Colorado School of Medicine at Denver, Aurora, CO 80045); Wiles TA ( Department of Immunology and Microbiology, University of Colorado School of Medicine at Denver, Aurora, CO 80045); Lindsay RS ( Department of Immunology and Microbiology, University of Colorado School of Medicine at Denver, Aurora, CO 80045); Barbour G ( Department of Immunology and Microbiology, University of Colorado School of Medicine at Denver, Aurora, CO 80045); Delong T ( Department of Immunology and Microbiology, University of Colorado School of Medicine at Denver, Aurora, CO 80045); Friedman RS ( Department of Immunology and Microbiology, University of Colorado School of Medicine at Denver, Aurora, CO 80045); Haskins K ( Department of Immunology and Microbiology, University of Colorado School of Medicine at Denver, Aurora, CO 80045)
Abstract	T cells reactive to ß cell Ags are critical players in the development of autoimmune type 1 diabetes. Using a panel of diabetogenic CD4 T cell clones derived from the NOD mouse, we recently identified the ß cell secretory granule protein, chromogranin A (ChgA), as a new autoantigen in type 1 diabetes. CD4 T cells reactive to ChgA are pathogenic and rapidly transfer diabetes into young NOD recipients. We report in this article that NOD.ChgA(-/-) mice do not develop diabetes and show little evidence of autoimmunity in the pancreatic islets. Using tetramer analysis, we demonstrate that ChgA-reactive T cells are present in these mice but remain naive. In contrast, in NOD.ChgA(+/+) mice, a majority of the ChgA-reactive T cells are Ag experienced. Our results suggest that the presence of ChgA and subsequent activation of ChgA-reactive T cells are essential for the initiation and development of autoimmune diabetes in NOD mice.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	1
Volume Number	196
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2016-01-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Autoantigens Immunology Cd4-positive T-lymphocytes Chromogranin A Genetics Diabetes Mellitus, Type 1 Adoptive Transfer Animals Autoimmunity B-lymphocytes Transplantation Cd8-positive T-lymphocytes Cells, Cultured Flow Cytometry Islets Of Langerhans Mice Mice, Inbred Balb C Mice, Inbred C57bl Mice, Inbred Nod Mice, Knockout Microsatellite Repeats Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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