Please help us congratulate Gregory Takacs and Dr. Jeffrey Harrison on their recent publication titled “Glioma-derived CCL2 and CCL7 mediate migration of immune suppressive CCR2+/CX3CR1+ M-MDSCs into the tumor microenvironment in a redundant manner”.
The study determined that CCR2 and its cognate ligands are prominent regulators of the recruitment of a CCR2+/CX3CR1+ immune suppressive cell to gliomas. The expression and functional characterization of these chemokine receptors further defines the M-MDSC phenotype. CCL2 and CCL7 are produced, at least in part, by glioma cells and our study indicates that CCL2 and CCL7 function in a redundant manner to induce the migration of CCR2+/CX3CR1+ M-MDSCs into the glioma microenvironment. As such, a more effective approach to limiting this population from gaining access to the TME should involve antagonizing CCR2. However, given that high CCL2 and CCL7 expression is associated with poorer prognosis in GBM patients, consideration of the relative expression of these two chemokines may provide predictive value to a therapeutic strategy targeting this chemokine:chemokine receptor axis.