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 5
scαCTLA-4 Tg⁺ B cells inhibit T cell–dependent B cell IgG2a Ab production in vivo. scαCTLA-4 Tg and FVB littermate control B cells were activated in the presence of LPS (1 μg/ml) for 72 hours, loaded with DNP-OVA, and transferred to naive FVB recipients. Seven days following transfer of cells, recipient animals were boosted with 100 μg DNP-OVA in CFA injected subcutaneously. Fourteen days following B cell transfer, anti-DNP Ab production was measured using DNP-KLH–specific ELISA. Shown in A, anti-DNP serum IgG2a from 4 individual WT or scαCTLA-4 Tg⁺–treated mice. (B) Anti-DNP serum IgG1 from 4 individual WT or scαCTLA-4 Tg⁺–treated mice. (C) Total Ig from 10 individual WT or scαCTLA-4 Tg⁺–treated mice. The mean for each group is shown with a horizontal line. Results shown are representative of at least 2 independent experiments.