| First Author | Bevaart L | Year | 2006 |
| Journal | Cancer Res | Volume | 66 |
| Issue | 3 | Pages | 1261-4 |
| PubMed ID | 16452176 | Mgi Jnum | J:106686 |
| Mgi Id | MGI:3619206 | Doi | 10.1158/0008-5472.CAN-05-2856 |
| Citation | Bevaart L, et al. (2006) The high-affinity IgG receptor, FcgammaRI, plays a central role in antibody therapy of experimental melanoma. Cancer Res 66(3):1261-4 |
| abstractText | We examined the role of FcgammaR in antibody therapy of metastatic melanoma in wild-type and different FcgammaR knock-out mice. Treatment of B16F10-challenged wild-type mice with TA99 antibody specific for the gp75 tumor antigen resulted in a marked decrease in numbers of lung metastases. Treatment of individual FcgammaR knock-out mice revealed the high-affinity IgG receptor, FcgammaRI (CD64), to represent the central FcgammaR for TA99-induced antitumor effects. The potential of immune-modulating agents to further enhance the protective effect induced by monoclonal antibody (mAb) TA99 was examined in combination treatments consisting of mAb TA99 and a TLR-4 agonist, monophosphoryl lipid A (MPL). MPL did potently boost TA99 antibody-induced effects, and combination therapy was, again, found to be dependent on the presence of FcgammaRI. |
