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West Ashley Library
Closed for Staff Day
Phone: (843) 766-6635
Wando Mount Pleasant Library
Closed for Staff Day
Phone: (843) 805-6888
Village Library
Closed for Staff Day
Phone: (843) 884-9741
St. Paul's/Hollywood Library
Closed for Staff Day
Phone: (843) 889-3300
Otranto Road Library
Closed for Staff Day
Phone: (843) 572-4094
Mt. Pleasant Library
Closed for Staff Day
Phone: (843) 849-6161
McClellanville Library
Closed for Staff Day
Phone: (843) 887-3699
Keith Summey North Charleston Library
Closed for Staff Day
Phone: (843) 744-2489
John's Island Library
Closed for Staff Day
Phone: (843) 559-1945
Hurd/St. Andrews Library
Closed for Staff Day
Phone: (843) 766-2546
Folly Beach Library
Closed for Staff Day
Phone: (843) 588-2001
Dorchester Road Library
Closed for Staff Day
Phone: (843) 552-6466
John L. Dart Library
Closed for Staff Day
Phone: (843) 722-7550
Baxter-Patrick James Island
Closed for Staff Day
Phone: (843) 795-6679
Main Library
Closed for Staff Day
Phone: (843) 805-6930
Bees Ferry West Ashley Library
Closed for Staff Day
Phone: (843) 805-6892
Miss Jane's Building (Edisto Library Temporary Location)
Closed
Phone: (843) 869-2355
Edgar Allan Poe/Sullivan's Island Library
Closed for renovations
Phone: (843) 883-3914
Mobile Library
9 a.m. - 5 p.m.
Phone: (843) 805-6909
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Granzyme A Deficiency Breaks Immune Tolerance and Promotes Autoimmune Diabetes Through a Type I Interferon-Dependent Pathway.
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- Author(s): Mollah, Zia U. A.; Hong Sheng Quah; Graham, Kate L.; Jhala, Gaurang; Krishnamurthy, Balasubramanian; Dharma, Joanna Francisca M.; Chee, Jonathan; Trivedi, Prerak M.; Pappas, Evan G.; Mackin, Leanne; Chu, Edward P. F.; Akazawa, Satoru; Fynch, Stacey; Hodson, Charlotte; Deans, Andrew J.; Trapani, Joseph A.; Chong, Mark M. W.; Bird, Phillip I.; Brodnicki, Thomas C.; Thomas, Helen E.
- Source:
Diabetes; Dec2017, Vol. 66 Issue 12, p3041-3050, 10p, 4 Graphs- Subject Terms:
- Source:
- Additional Information
- Abstract: Granzyme A is a protease implicated in the degradation of intracellular DNA. Nucleotide complexes are known triggers of systemic autoimmunity, but a role in organ-specific autoimmune disease has not been demonstrated. To investigate whether such a mechanism could be an endogenous trigger for autoimmunity, we examined the impact of granzyme A deficiency in the NOD mouse model of autoimmune diabetes. Granzyme A deficiency resulted in an increased incidence in diabetes associated with accumulation of ssDNA in immune cells and induction of an interferon response in pancreatic islets. Central tolerance to proinsulin in transgenic NOD mice was broken on a granzyme A-deficient background. We have identified a novel endogenous trigger for autoimmune diabetes and an in vivo role for granzyme A in maintaining immune tolerance. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Diabetes is the property of American Diabetes Association and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Abstract:
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