AEA has been shown to exert an inhibitory impact on chemokine elicited lymphocyte migration. The inhibition of stromal derived factor 1 induced migration of CD8 T lymphocytes was observed to be mediated through the CB2. But, there also are studies that AEA may use effects. It’s been noted that AEA acts as a complete growth factor for primary murine marrow cells and hematopoietic growth factor dependent cell lines. ALK inhibitor AEA also has been found to increase production of IL 6 by astrocytes which have been infected with Theiler s murine encephalomyelitis virus. But, in these studies the effect of AEA was shown to be blocked by the CB1 antagonist SR141716A suggesting involvement of the CB1, as opposed to the CB2, in the elevation of ranges of this pleiotropic cytokine. As opposed to AEA, 2 AG has been associated primarily with enhancement of immune responses. It’s been reported that 2 AG stimulates the release of nitric oxide from human Ribonucleic acid (RNA) immune and vascular cells and from invertebrate immunocytes by way of a style that’s related to CB1 and that hematopoietic cells expressing CB2 move in response to 2 AG. Different profiles for CB2 expression in lymphoid cells have been reported to be dependent on the state of receptor activation, and it has been proposed that cell migration takes its major function of CB2 upon stimulation with 2 AG. Furthermore, it has been shown that 2 AG triggers the migration of human peripheral blood monocytes and promyelocytic leukemia HL60 cells that have been classified into macrophage like cells. This activity has been implicated as developing via a CB2 dependent mechanism. Subsequent studies have demonstrated that 2 AG triggers accelerated production of chemokines from the HL 60 cells. Moreover, rat microglia have been reported to synthesize 2 AG in vitro, a function that’s been attributed as associated with increased growth by way of a CB2 dependent mechanism. Position of CB2 In Neuroinflammation The early studies that CTEP were done to determine the practical importance of CB1 and CB2 suggested while the appearance of the CB2 was limited to cells and tissues of the immune system that the CB1 was compartmentalized to the CNS. The development of phenotypically normal CB2 knockout mice was an important development that contributed to elucidation of the part of CB2 in immune modulation inside the CNS. In addition to the CB2 knockout mouse strain developed by colleagues and Buckley, Deltagen developed a CB2 knockout mouse strain that is commercially available through Jackson Laboratories. These CB2 knock-out mice strains have mutations in the carboxy and amino termini, respectively. The tissues from these mice have been applied extensively in studying CB2 mediated responses and CB2 function.