Inhibition of T cell activation and autoimmune diabetes using a B cell surface–linked CTLA-4 agonist
J. Clin. Invest. Brian T. Fife, et al. 116:2252 doi:10.1172/JCI27856 [Go to this article.]

Figure 8
scαCTLA-4 Tg⁺ B cells inhibit the activation of autoreactive T cells in pancreatic lymph nodes. BDC2.5.Thy1.1 CD4⁺ LN cells were labeled with CFSE and adoptively transferred to prediabetic 6-week-old NOD.B7 DKO or NOD.B7 DKO.scαCTLA-4 Tg⁺ mice. Pancreatic and inguinal LN cells were harvested from recipients (n = 3 for each group) 5 days later for analysis by flow cytometry for CFSE dye dilution as a readout of in vivo priming and proliferation. (A) Representative histogram CFSE plots of CD4⁺CD90.1⁺ T cells from NOD.B7 DKO and NOD.B7 DKO.scαCTLA-4 Tg⁺ recipients. (B) Direct assessment of in vivo differentiation and IFN-γ production measured by flow cytometry ex vivo. CD4⁺CD25^– T cells from BDC2.5.Thy1.1.Yeti mice transferred to prediabetic NOD.B7 DKO or NOD.B7 DKO.scαCTLA-4 recipients (n = 3 for each group). Shown here is YFP (IFN-γ) and CD62L expression from CD4⁺CD90.1⁺ T cells from pancreatic and inguinal LNs. Results shown are representative of 2 independent experiments.