Figure 5. Supplementation with IL-2... | Rockefeller University Press

Figure 5.

$Figure 5. Supplementation with IL-2 induces early IFN-γ production and eventual accumulation of NK cells in the pancreatic lesion, as well as clinical diabetes. Pancreatic infiltrate from BDC2.5/NOD mice was analyzed 24 h after treatment with control PBS, IL-2–S4B6 complexes, or mutant IL-2 analogue Super-2, or 4 d after injection of IL-2–S4B6 complexes. (A, left) Representative flow cytometry data. (middle) Summary data for fraction of NK cells in the FSC/SSC lymphocyte gate. (right) Cell number summary data. (B) Analogous data for IFN-γ–producing NK cells. Mean ± SD, at least three independent experiments for both panels. (C) Summary diabetes data for 2 cohorts after 3 consecutive treatments with IL-2–S4B6 complexes (n = 14 IL-2–S4B6 complex; n = 9 PBS).$

Supplementation with IL-2 induces early IFN-γ production and eventual accumulation of NK cells in the pancreatic lesion, as well as clinical diabetes. Pancreatic infiltrate from BDC2.5/NOD mice was analyzed 24 h after treatment with control PBS, IL-2–S4B6 complexes, or mutant IL-2 analogue Super-2, or 4 d after injection of IL-2–S4B6 complexes. (A, left) Representative flow cytometry data. (middle) Summary data for fraction of NK cells in the FSC/SSC lymphocyte gate. (right) Cell number summary data. (B) Analogous data for IFN-γ–producing NK cells. Mean ± SD, at least three independent experiments for both panels. (C) Summary diabetes data for 2 cohorts after 3 consecutive treatments with IL-2–S4B6 complexes (n = 14 IL-2–S4B6 complex; n = 9 PBS).