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Phone: (843) 766-6635
Wando Mount Pleasant Library
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Phone: (843) 805-6888
Village Library
Closed for Staff Day
Phone: (843) 884-9741
St. Paul's/Hollywood Library
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Phone: (843) 889-3300
Otranto Road Library
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Phone: (843) 572-4094
Mt. Pleasant Library
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Phone: (843) 849-6161
McClellanville Library
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Keith Summey North Charleston Library
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John's Island Library
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Hurd/St. Andrews Library
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Folly Beach Library
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Dorchester Road Library
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John L. Dart Library
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Baxter-Patrick James Island
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Main Library
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Bees Ferry West Ashley Library
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Miss Jane's Building (Edisto Library Temporary Location)
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Immunomodulation Followed by Antigen-Specific Treg Infusion Controls Islet Autoimmunity.
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- Author(s): Cabello-Kindelan, Cecilia; Mackey, Shane; Sands, Alexander; Rodriguez, Jennifer; Vazquez, Claudia; Pugliese, Alberto; Bayer, Allison L.
- Source:
Diabetes; Feb2020, Vol. 69 Issue 2, p215-227, 13p, 1 Chart, 6 Graphs- Subject Terms:
SUPPRESSOR cells; IMMUNOREGULATION; TYPE 1 diabetes; ISLANDS of Langerhans; T cells; IMMUNOLOGICAL tolerance; RESEARCH; SKIN grafting; ANIMAL experimentation; RESEARCH methodology; IMMUNE system; CELL physiology; EVALUATION research; MEDICAL cooperation; COMPARATIVE studies; IMMUNITY; RESEARCH funding; MICE - Source:
- Additional Information
- Abstract: Optimal immune-based therapies for type 1 diabetes (T1D) should restore self-tolerance without inducing chronic immunosuppression. CD4+Foxp3+ regulatory T cells (Tregs) are a key cell population capable of facilitating durable immune tolerance. However, clinical trials with expanded Tregs in T1D and solid-organ transplant recipients are limited by poor Treg engraftment without host manipulation. We showed that Treg engraftment and therapeutic benefit in nonautoimmune models required ablative host conditioning. Here, we evaluated Treg engraftment and therapeutic efficacy in the nonobese diabetic (NOD) mouse model of autoimmune diabetes using nonablative, combinatorial regimens involving the anti-CD3 (αCD3), cyclophosphamide (CyP), and IAC (IL-2/JES6-1) antibody complex. We demonstrate that αCD3 alone induced substantial T-cell depletion, impacting both conventional T cells (Tconv) and Tregs, subsequently followed by more rapid rebound of Tregs Despite robust depletion of host Tconv and host Tregs, donor Tregs failed to engraft even with interleukin-2 (IL-2) support. A single dose of CyP after αCD3 depleted rebounding host Tregs and resulted in a 43-fold increase in donor Treg engraftment, yet polyclonal donor Tregs failed to reverse diabetes. However, infusion of autoantigen-specific Tregs after αCD3 alone resulted in robust Treg engraftment within the islets and induced remission in all mice. This novel combinatorial therapy promotes engraftment of autoantigen-specific donor Tregs and controls islet autoimmunity without long-term immunosuppression. [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.)
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