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. Author manuscript; available in PMC: 2018 Dec 13.
Published in final edited form as: Cancer Cell. 2018 Jun 11;33(6):1033–1047.e5. doi: 10.1016/j.ccell.2018.05.005

Figure 6. Fc-FcγR Co-engagement by Anti-CTLA-4 mAbs Modulates TCR Signaling.

Figure 6.

(A) Enforced cell surface expression of CTLA-4 by Jurkat IL-2-luc T cells and endogenous expression of CD80 and CD86 on Raji APCs as compared with isotype control mAbs (gray).

(B) Expression of FcγRs on Raji APCs, as compared with isotype control mAbs (gray).

(C) Jurkat IL-2-luc T cell reporter activation following 8 hr co-culture with Raji APCs in the presence of increasing doses of anti-CTLA-4 mAb variants or hIgG1 isotype control mAb. Error bars indicate SEM.

(D and E) Kinetic immunoblot analysis (D) and associated quantitative densitometry (E) of phosphorylated ZAP70 (Y-493) in human PBMCs following stimulation with 50 ng/mL of SEA peptide and 10 μg/mL of anti-CTLA-4 mAb variants (hIgG1, hIgG1-N297A, or hIgG1-DLE) or hIgG1 isotype control.

See also Figure S6.