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. 2020 Apr 9;10:6156. doi: 10.1038/s41598-020-62881-4

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Optimized LL-CFA/I therapy is protective at 30 wks. Four wk-old NOD females were orally dosed with 5 × 10⁷ CFUs of LL-CFA/I, LL vector, or PBS. Additional doses were given every 2 wks. (A) Blood glucose levels of individual mice treated with LL-CFA/I, LL vector, or PBS (n = 10/group) are depicted. Values above the dotted lines are considered hyperglycemic. (B) Summary of disease incidence of mice given the various treatments. Dotted line represents incidence of mice treated with LL-CFA/I. At 30 wks or when hyperglycemic mice were euthanized, (C) splenic and (D) PaLN lymphocytes were stimulated with anti-CD3 and anti-CD28 mAbs to assess extent of IL-10, TGF-β, IL-17, IL-13, and IL-4 production. Pancreatic lymphocytes were purified and analyzed for expression of (E) Foxp3 and Tbet expression; PBS (n = 5), LL vector (n = 5), and LL-CFA/I (n = 7). *p < 0.05 for LL-CFA/I vs PBS; ^#p < 0.05 for LL-CFA/I vs LL vector.