Stimulation of TNF‐R2 and CD40 enhances TNF‐R1‐induced cytotoxicity independently of endogenous TNF. (A) KYM‐1 cells were treated with the TNF‐R1‐specific mAb Htr‐1 in the absence (□) or presence (▪) of TNF‐R2‐specific polyclonal rabbit IgG M80 and cell viability was determined after 6 h by MTT assays. Stimulation of TNF‐R2 and CD40 enhances TNF‐R1‐induced cytotoxicity independently of endogenous TNF. (A) KYM‐1 cells were treated with the TNF‐R1‐specific mAb Htr‐1 in the absence (□) or presence (▪) of TNF‐R2‐specific polyclonal rabbit IgG M80 and cell viability was determined after 6 h by MTT assays. (B) KYM‐1 cells were incubated with anti‐human TNF mAb 357‐101‐4 (30 μg/ml) and then cultured for 18 h with titrated concentrations of TNF‐R1‐specific mAb Htr‐1 in the absence (□) or presence (▪) of TNF‐R2‐specific mAb MR2‐1 (0.1 μg/ml). (C) HeLa‐CD40 cells were incubated with neutralizing anti‐human TNF mAb 195 (30 μg/ml) and then cultured for 18 h with CHX (2.5 μg/ml) and titrated concentrations of TNF‐R1‐specific mAb Htr‐1 in the absence (□) or presence (▪) of CD40‐specific mAb G28.5 (1 μg/ml). Matthias Grell et al. EMBO J. 1999;18:3034-3043 © as stated in the article, figure or figure legend