Recombinant Mouse CCL9 (MIP-1gamma) (carrier-free)

Mouse CCL9 was initially cloned from cDNA libraries of BaF3 and RAW 264.7 cells. It is constitutively expressed in a big variety of tissues, including the follicle-associated epithelium overlaying the dome regions of the Peyer’s patches. Using CCR6 -/- mice, it was shown that CCL9 recruits CD11b+ dendritic cells (DCs) to the sub-epithelial dome regions of the Peyer’s patch. This data showed that the CCL20/CCR6 pair is not absolutely required for the recruitment of CD11b+ DCs to that region. In addition, CCL9 is induced in Raw264.7 and bone marrow cells by RANKL, and the use of this osteoclastogenesis model suggested that CCL9 stimulates the activation and survival of mature osteoclasts. The expression of CCL9 and CCR1 in osteoclasts suggests a role for CCL9 in bone resorption. Additional data have shown that activation of TLR-9 in microglia with unmethylated CpG oligodeoxynucleotides (CpG-ODNs) induces production of CCL9 and expression of CCR1. In addition, Retinoid X Receptor alpha (RXRa) plays a role in the regulation of the innate immune response, and the disruption of this nuclear receptor, in peritoneal macrophages, induces a decrease in CCL6 and CCL9 in vivo, correlating with impaired leukocyte recruitment to inflammatory sites and prolonged survival in sepsis.