Fig. 7
Anti-CD3 mAb and IGRP therapy delays the autoimmune progression of T1D. A Experimental design for adoptive transfer studies. NOD SCID mice aged 8–10 weeks underwent an adoptive transfer of CD8+CD44+PD-1− T cells derived from NY8.3 mice aged 6–8 weeks. The recipient mice were treated with either 20 µg of IGRP206–214 per nostril daily for three consecutive days or 10 µg of anti-CD3 monoclonal antibody (mAb) daily for 5 days. On days 5 and 15 post-treatment, the mice were sacrificed. Quantitative analysis and flow cytometry data of total exhausted CD8+ T cells, as well as TPEX and TEX cells were collected on days 5 (B) (n = 6/group) and 15 (C) (n = 6/group). D Experimental design for NY8.3 mice immunotherapy studies. Four-week-old female NY8.3 mice (n = 16/group) were treated with 10 mg anti-CD3mAb or 20 µg IGRP206–214 per nostril daily for 3 days. Mice were sacrificed at day 40 after treatment. E The prevalence of diabetes during the course of treatment in NY8.3 mice. F At day 40, the percentage of pancreatic islets exhibiting the specified histological scores in “non-diabetic” mice from D was measured. For insulitis, ten pieces per pancreas were blindly scored. (0 = no infiltrate, 1 = 0–25%, 2 = 25–75%, 3 ≥ 75%). White bars, 0; light grey bars, 1; dark grey bars, 2; black bars, 3. Representative pictures of the islets at day 40 “non-diabetic” mice from D. Mann–Whitney test (B,C); one-way ANOVA (E). Scale bars, 50 μm