| First Author | Dyall R | Year | 1999 |
| Journal | Eur J Immunol | Volume | 29 |
| Issue | 1 | Pages | 30-7 |
| PubMed ID | 9933083 | Mgi Jnum | J:52267 |
| Mgi Id | MGI:1328703 | Doi | 10.1002/(SICI)1521-4141(199901)29:01<30::AID-IMMU30>3.0.CO;2-D |
| Citation | Dyall R, et al. (1999) Cellular requirements for the monoclonal antibody-mediated eradication of an established solid tumor. Eur J Immunol 29(1):30-7 |
| abstractText | Following subcutaneous implantation, the murine lymphoma E.G7 [a variant of EL-4, transfected with the chicken ovalbumin (OVA) gene] up-regulates the CD4 molecule. We previously showed that the administration of an anti-CD4 monoclonal antibody (mAb) to EG.7-bearing mice leads to a rapid and complete regression of large established tumors. This tumor regression was shown to require both CD8+ cells and functional Fcgamma receptors (FcgammaR), as it failed to occur in mice depleted of CD8 cells, or mice genetically deficient in FcgammaI/III (gamma-/-mice). Using adoptive transfer, we now show that the FcgammaR+ cells required for this regression are the CD11b+ (phagocytic) cells. Furthermore, experiments using peptide tolerization demonstrated that the critical CD8 CTL population in this model is tumor specific. Analysis of tumors at various stages of regression revealed a massive CD11b+FcgammaR+ and a marginal CD8 infiltration. In the presence of the CTL determinant OVA-8 on tumor cells and of the antitumor mAb, this CD8 infiltration became remarkable, and correlated with tumor regression. These results identify the specific cellular effectors essential for the mAb-mediated tumor regression, and suggest that FcgammaR-activated macrophages induced an expansion of tumor-eliminating CTL in situ. |
