Does tGFβ signaling play a critical role in promoting alternative macrophage activation?
Our results establish a novel biological role for TGFβ signaling in controlling expression of genes characteristic for alternatively activated macrophages. We speculate that lack of TβRII signaling reduces the anti-inflammatory M2 phenotype of macrophages because of reduced expression of these products. This would cause defects in the ability of the M2 macrophages to negatively regulate other immune cells such as T-cells in the lung, possibly explaining the systemic inflammation observed in Vav1-Cre x TβRIIfx/fx mice.
Growth hormone attenuated the positive APR, as indicated by a decrease in alpha 1-acid glycoprotein expression and production, and prevented the negative APR, as seen by an absence of a decline of albumin mRNA pool levels and serum concentration. We conclude that the beneficial effects of GH on thermal injury may be due in part to a modification of the APR.