| First Author | Li F | Year | 2013 |
| Journal | Proc Natl Acad Sci U S A | Volume | 110 |
| Issue | 48 | Pages | 19501-6 |
| PubMed ID | 24218606 | Mgi Jnum | J:203058 |
| Mgi Id | MGI:5524171 | Doi | 10.1073/pnas.1319502110 |
| Citation | Li F, et al. (2013) Antitumor activities of agonistic anti-TNFR antibodies require differential FcgammaRIIB coengagement in vivo. Proc Natl Acad Sci U S A 110(48):19501-6 |
| abstractText | Agonistic anti-TNF receptor (TNFR) superfamily member antibodies are a class of promising antitumor therapies in active clinical investigation. An unexpected requirement for inhibitory Fcgamma receptor FcgammaRIIB coengagement has recently been described for their in vivo antitumor activities. Although these findings have informed the design of more potent antitumor agonistic, anti-TNFR therapies, the underlying mechanism has remained obscure. Through detailed genetic analysis of strains conditionally deleted for FcgammaRIIB on defined cellular populations or mutated in specific signaling components, we now demonstrate that different agonistic anti-TNFR antibodies have specific requirements for FcgammaRIIB expression on defined cellular populations and function in trans in the absence of FcgammaRIIB signaling components, thus supporting a general mechanism of FcgammaRIIB cross-linking in vivo for the activities of these antibodies. |
