Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 1261-4 |
| Number of pages | 4 |
| Journal | Cancer Research |
| Volume | 66 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 1 Feb 2006 |
Keywords
- Animals
- Antibodies, Monoclonal
- Antibody Specificity
- Immunization, Passive
- Lipid A
- Lung Neoplasms
- Melanoma, Experimental
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Receptors, IgG
- Journal Article
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