RT Journal Article
SR Electronic
T1 Lung Tumor Growth is Stimulated in IFN-γ<sup>−/−</sup> Mice and Inhibited in IL-4Rα<sup>−/−</sup> Mice
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 5095
OP 5101
VO 29
IS 12
A1 ELIZABETH F. REDENTE
A1 LORI D. DWYER-NIELD
A1 BRADLEY S. BARRETT
A1 DAVID W.H. RICHES
A1 ALVIN M. MALKINSON
YR 2009
UL http://ar.iiarjournals.org/content/29/12/5095.abstract
AB Background: Alternative (M2) macrophage activation is associated with tumor development in many tumor types, including those in the lung. Herein the biological consequences of forcing classical (M1) or alternative (M2) macrophage activation on lung tumor development are examined. Materials and Methods: Urethane-induced lung tumor multiplicity and size were compared in IFN-γ−/− mice which lack M1 macrophage activation, IL-4Rα−/− mice which lack M2 macrophage activation, and wild-type BALB/cJ (background strain of the IFN-γ−/− and IL-4Rα−/− mice) mice. Tumor-associated macrophage (TAM) and bone marrow-derived monocyte (BDMC) activation were each examined. Results: The TAMs and BDMCs in the IFN-γ−/− mice exhibited M2 activation, and their lung tumors were significantly larger than those in the wild-type mice. In contrast, urethane-treated IL-4Rα−/− mice, whose TAMs and BDMCs were M1 activated, developed smaller tumors than the wild-type mice. Conclusion: Altered innate immunity can diminish or accelerate lung tumor progression in response to defective cytokine signaling.