The important anatomical features of the CNS include the following: lack of lymphatic drainage from the parenchyma; lack of endogenous antigenpresenting cells; and the blood-brain barrier or blood-spinal cord barrier, which restricts the access of soluble factors to the CNS and limits the access of immune cells to the site. However, immune cells such as neutrophils, macrophages, T cells, and dendritic cells may infiltrate brain parenchyma after injury to the CNS, by penetrating breaks in the BBB or BSCB. Once immune cells have infiltrated the CNS, they may release reactive oxygen species, nitrogen oxide, free radicals, and proteases, which can exacerbate tissue damage. Leukocytes that have infiltrated the CNS also release cytokines and chemokines, which activate the resident microglia or bloodderived monocytes to participate in the immune response at the injured sites. In contrast, activated microglia and macrophages play both beneficial and harmful roles in the injured CNS. Under inflammatory conditions, extrinsic cells such as neutrophils, macrophages, T cells, and DCs interact with resident microglia to maintain equilibrium between the injured CNS and the immune system. T cells are considered harmful to the injured CNS after traumatic brain injury. However, T cells may also have neuroprotective effects, which contribute to repair. Under an inflammatory milieu in the CNS, APCs interact with meningeal T cells, which home to cervical lymph nodes via lymphatic vessels. Several studies have shown that antigen carrying DCs participate in restricting damage to the nervous system after trauma to the CNS and during the process of postinjury repair. DCs emigrating from the brain have been shown to infiltrate peripheral lymphatic organs, inducing a local immune response and directing antigen-specific T cells back to the brain. Notably, in rodents and ruminants. In addition, myelin antigens presented by DCs have been detected in the CLNs of a primate model of an inflammatory demyelinating disorder. Although previous studies measured mixed populations consisting of microglia and macrophages, this study assessed each of these 2 distinct populations separately, according to the intensity of CD45/CD11b immunofluorescence. Neutrophils and macrophages strongly infiltrated the brain in the early phase of CCI, as would be expected on the basis of previous studies in a TBI model. However, this study identified that microglia in the injured brain first ABT-199 increased and then reached a peak at 1 week after CCI, which was followed by a second surge after 2 weeks. A reduction in microglia in the injured brain was observed 1 d after CCI, followed by a bimodal increase at 1 week and in the chronic phase. This increase was predominantly found around the injury site. Iba1 staining of injured brain sections showed that microglia were morphologically round at 1 week after injury, whereas those at 3 weeks were more ramified, suggesting that different subtypes of microglia were dominant between 1 and 3 weeks after injury. Indeed, cell surface marker analysis showed that M2-like microglia peaked at 1 week and M1-like microglia increased at 4 weeks. However, more than 70% of microglia were CD862/ CD2062. Studying other markers for M1 and M2 might be necessary to appropriately classify microglia in the brain, or unknown subsets of microglia might differentiate from resting state microglia after CCI. Complete characterization of microglia will be required to elucidate the function of these cells. Interestingly, the dynamic changes seen in the number of T cells in the CLNs showed a similar pattern, with a 1-week delay, to that of microglia in the injured brain.