After IV infection, pulmonary CD103+ DCs are expanded and activated and their migration and antigen (Ag) presentation to the draining mediastinal lymph nodes is mediated by GM-CSF.
Injection of GM-CSF-activated monocytes was not able to protect Rag1-deficient mice against DSS-induced colitis, indicating that adaptive immunity is required for the protection mediated by GM-CSF-activated monocytes [16].
Thus, we recorded higher net photosynthetic rate (AN) values under saline conditions and 700 ppm CO2, being this effect mainly mediated by a reduction of mesophyll (gm) and biochemical limitation imposed to salt excess.
We hypothesized that this singularity could be mediated by granulocyte-macrophage colony-stimulating factor (GM-CSF) (known to be predominantly produced by type II pneumocytes) and interferon-gamma (INFγ), two cytokines known to prevent the occurrence of ET [ 3].
They are mediated by the growth factors G-CSF and GM-CSF (s. Appendix A1.1) [ 35- 37].
To show the mechanism underlying the enhanced antitumor effect mediated by vaccine co-expression IL-18 and GM-CSF, we next detected the expression of Th1 or Th2 cytokine in serum.
The greater recovery of Lin- BM cells in the Nf1−/− mice is likely indicative of chronic polyclonal hyperproliferation due to hypersensitivity to GM-CSF, which is mediated by increased and prolonged Ras activation [ 30].
This interface, termed interface V, is mediated by the loop region between helix A and helix B of GM-CSF bound to two different hexamers.
In addition to constitutive apoptosis, inducible apoptosis mediated by the Fas pathway is suppressed by a variety of inflammatory mediators, including IL-8 [ 149], G-CSF, GM-CSF, interferon-γ, and TNF-α [ 150].
GM-associated nephrotoxicity is considered a tubulopathy-inducing renal insufficiency mediated by tubular damage and dysfunction.
In vitro studies of decidualized human stromal cells revealed that steroid hormone withdrawal increased a host of inflammatory mediators, including IL-6, CCL11, GM-CSF, CCL2, IL1-RA, CXCL10 and CXCL8, and this response was mediated by NF-κB (Evans and Salamonsen, 2014).
