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Neuron|September 15, 2020
Sensory Experience Engages Microglia to Shape Neural Connectivity through a Non-Phagocytic MechanismLucas Cheadle, Samuel A Rivera, Jasper S Phelps, et al.
Proceedings of the National Academy of Sciences of the United States of America|October 17, 2012
Microglial repopulation model reveals a robust homeostatic process for replacing CNS myeloid cellsNicholas H Varvel, Stefan A Grathwohl, Frank Baumann, et al.
Biorxiv : the Preprint Server for Biology|December 22, 2025
Conserved phenotype and function of human brain border-associated macrophages in iPSC-derived modelsHelena J Barr, Constanze Depp, Maximilian Hingerl, et al.
Nature Neuroscience|February 22, 2018
Microglia-mediated recovery from ALS-relevant motor neuron degeneration in a mouse model of TDP-43 proteinopathyKrista J Spiller, Clark R Restrepo, Tahiyana Khan, et al.
Oncotarget|May 20, 2015
Loss of CX3CR1 increases accumulation of inflammatory monocytes and promotes gliomagenesisXi Feng, Frank Szulzewsky, Alexan Yerevanian, et al.
Science Translational Medicine|July 7, 2017
Glucose-regulated protein 78 autoantibody associates with blood-brain barrier disruption in neuromyelitis opticaFumitaka Shimizu, Kristin L Schaller, Gregory P Owens, et al.
Proceedings of the National Academy of Sciences of the United States of America|September 7, 2007
Disrupted cardiac development but normal hematopoiesis in mice deficient in the second CXCL12/SDF-1 receptor, CXCR7Frederic Sierro, Christine Biben, Laura Martínez-Muñoz, et al.
Journal of Neurotrauma|September 29, 2015
Altered Neuroinflammation and Behavior after Traumatic Brain Injury in a Mouse Model of Alzheimer's DiseaseOlga Kokiko-Cochran, Lena Ransohoff, Mike Veenstra, et al.
FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology|May 6, 2006
The neuronal chemokine CX3CL1/fractalkine selectively recruits NK cells that modify experimental autoimmune encephalomyelitis within the central nervous systemDeRen Huang, Fu-Dong Shi, Steffen Jung, et al.
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