A role for TREM2 ligands in the phagocytosis of apoptotic neuronal cells by microglia. Hsieh CL, Koike M, Spusta SC, Niemi EC, Yenari M, Nakamura MC, et al. TREM2 deficiency eliminates TREM2+ inflammatory macrophages and ameliorates pathology in Alzheimer’s disease mouse models. Jay TR, Miller CM, Cheng PJ, Graham LC, Bemiller S, Broihier ML, et al. Attenuated inflammatory response in triggering receptor expressed on myeloid cells 2 (TREM2) knock-out mice following stroke. Sieber MW, Jaenisch N, Brehm M, Guenther M, Linnartz-Gerlach B, Neumann H, et al. Triggering receptor expressed on myeloid cells 2 (TREM2) deficiency attenuates phagocytic activities of microglia and exacerbates ischemic damage in experimental stroke. Kawabori M, Kacimi R, Kauppinen T, Calosing C, Kim JY, Hsieh CL, et al. Altered microglial response to Abeta plaques in APPPS1-21 mice heterozygous for TREM2. Ulrich JD, Finn MB, Wang Y, Shen A, Mahan TE, Jiang H, et al. Triggering receptor expressed on myeloid cells-2 is involved in prion-induced microglial activation but does not contribute to prion pathogenesis in mouse brains. Zhu C, Herrmann US, Li B, Abakumova I, Moos R, Schwarz P, et al. Distribution and signaling of TREM2/DAP12, the receptor system mutated in human polycystic lipomembraneous osteodysplasia with sclerosing leukoencephalopathy dementia. Sessa G, Podini P, Mariani M, Meroni A, Spreafico R, Sinigaglia F, et al. Clearance of apoptotic neurons without inflammation by microglial triggering receptor expressed on myeloid cells-2. Cutting edge: inhibition of TLR and FcR responses in macrophages by triggering receptor expressed on myeloid cells (TREM)-2 and DAP12. Hamerman JA, Jarjoura JR, Humphrey MB, Nakamura MC, Seaman WE, Lanier LL. TREM and TREM-like receptors in inflammation and disease. Microglial and macrophage polarization-new prospects for brain repair. Hu X, Leak RK, Shi Y, Suenaga J, Gao Y, Zheng P, et al. Chronic treatment with minocycline preserves adult new neurons and reduces functional impairment after focal cerebral ischemia. Liu Z, Fan Y, Won SJ, Neumann M, Hu D, Zhou L, et al. Inflammation is detrimental for neurogenesis in adult brain. Epub 3.Įkdahl CT, Claasen JH, Bonde S, Kokaia Z, Lindvall O. M2 microglia and macrophages drive oligodendrocyte differentiation during CNS remyelination. Miron VE, Boyd A, Zhao JW, Yuen TJ, Ruckh JM, Shadrach JL, et al. Contribution of macrophages to enhanced regenerative capacity of dorsal root Ganglia sensory neurons by conditioning injury. Kwon MJ, Kim J, Shin H, Jeong SR, Kang YM, Choi JY, et al. Long-term accumulation of microglia with proneurogenic phenotype concomitant with persistent neurogenesis in adult subventricular zone after stroke. Thored P, Heldmann U, Gomes-Leal W, Gisler R, Darsalia V, Taneera J, et al. Heme oxygenase-1 exacerbates early brain injury after intracerebral haemorrhage. Neurobiology of microglial action in CNS injuries: receptor-mediated signaling mechanisms and functional roles. Hu X, Liou AK, Leak RK, Xu M, An C, Suenaga J, et al. Resting microglia directly monitor the functional state of synapses in vivo and determine the fate of ischemic terminals. Wake H, Moorhouse AJ, Jinno S, Kohsaka S, Nabekura J. Evidence for synaptic stripping by cortical microglia. Trapp BD, Wujek JR, Criste GA, Jalabi W, Yin X, Kidd GJ, et al. Microglia: active sensor and versatile effector cells in the normal and pathologic brain. Microglial cell origin and phenotypes in health and disease. The origin and cell lineage of microglia: new concepts. Kettenmann H, Hanisch UK, Noda M, Verkhratsky A. Further identification of the microglial receptors and/or signaling pathways that are in charge of functional phenotype switch is essential for the research in the stroke field and for the identification of therapeutic targets. We also discuss the different roles of activated microglia in ischemic brain injury and post-injury brain repair. In this review, we describe the main surface receptors that involve in microglial activation after stroke, with a focus on their engagement of distinct functional programs. Upon activation, these highly plastic cells may assume diverse phenotypes and play dualistic roles in brain injury and recovery. Microglia express a wide range of surface receptors, which control the “On” or “Off” responses of microglia and maintain their functional homeostasis. They serve as the first line of defense against CNS injuries such as ischemic stroke. Microglia are the residential immune cells in the central nervous system (CNS).

Double sided sword after earth