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Publication : Potentiation of antitumor CTL response by GM-CSF involves a B7-dependent mechanism.

First Author  Mokyr MB Year  1997
Journal  Cell Immunol Volume  178
Issue  2 Pages  152-61
PubMed ID  9225006 Mgi Jnum  J:41479
Mgi Id  MGI:893957 Doi  10.1006/cimm.1997.1130
Citation  Mokyr MB, et al. (1997) Potentiation of antitumor CTL response by GM-CSF involves a B7-dependent mechanism. Cell Immunol 178(2):152-61
abstractText  We have previously demonstrated the importance of endogenous GM-CSF production for the B7-2-dependent potentiating effect of exogenous TNF for CTL generation by stimulation cultures of splenic cells from mice bearing a large MOPC-315 tumor. Here we show that addition of GM-CSF to stimulation cultures of such tumor-bearer splenic cells also leads to the generation of enhanced anti-MOPC-315 CTL activity via a B7-dependent mechanism. However, while the potentiating effect of TNF was previously shown to be IL-2-independent, the potentiating effect of GM-CSF is shown here to be completely IL-2-dependent. Still, the potentiating activity of exogenous GM-CSF for the in vitro generation of CTL activity is shown to depend completely on endogenous TNF production. Finally, TNF and GM-CSF may cooperate in enhancing the in vivo generation of CTL activity in MOPC-315 tumor bearers because low-dose melphalan (L-phenylalanine mustard) therapy, which was previously shown to lead to the rapid up-regulation of TNF production at the tumor site and the subsequent TNF-dependent in vivo acquisition of potent CTL activity, is shown here to lead to the rapid up-regulation of GM-CSF production at the tumor site.
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