By M. Baggiolini (auth.), P. M. Murphy, R. Horuk (eds.)
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Additional resources for Chemokine Roles in Immunoregulation and Disease
1998). The finding that the CX3 CLl receptor, CX3CR1, is preferentially localized on microglia has provoked the reasonable notion that CX3 CL1 plays an important role in neuron to microglia communication, which was supported by studies in a facial nerve axotomy model (Harrison et al. 1998). Thus, CX3 CLl and its receptor were highly upregulated at affected sites in the brain with motor neurons being the primary source of the chemokine while microglia expressed the receptor. Moreover, CX 3 CLI treatment of primary cultured rat microglial cells induced vigorous increases in intracellular ci+ levels and chemotaxis, which were inhibited by an antibody against the CX3CLl receptor, CX3 CRI (Harrison et al.
Thus, neuronal-glial communication was not impaired in the absence of the CX 3 CLI receptor in this model, suggesting interaction between neurons and microglia through CX 3CRI and its ligand is not pivotal in nerve injury. Clearly, and unlike CXCLl2, CX 3 CLl is dispensable for normal CNS development and neuronal survival. Therefore, at present the function of CX3 CL1 in the CNS is uncertain and it would seem possibly more subtle than previously thought. L. Campbell CX3 CLl knock-out mice are less susceptible to cerebral ischemia-reperfusion injury (Soriano et al.
2002). Thus, agents that interrupt CCL2-mediated CCR2 signaling may be therapeutically useful in vascular disease. Multiple sclerosis (MS) may be another example of an inflammatory disease in which CCL2 plays an important pathogenetic role (Ransohoff et al. 1994). Genetic deletion of CCL2 or CCR2, or blockade by antibodies, dramatically reduces the severity of central nervous system disease in experimental allergic encephalomyelitis (EAE), a rodent model of MS (Fife et al. 2000; Izikson et al. 2000; Huang et al.