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Paper Details

Complement component 3 from astrocytes mediates retinal ganglion cell loss during neuroinflammation.
Acta Neuropathol
38
2021
-tdTomato reporter, C3, C3 gene variants, C3+/+, C3+/GFAP+ cells, C3-/-, Complement, Complement component 3, EAE, GFAP, MS, Multiple sclerosis, RBPMS, RBPMS+ cells, RGC, Retinal ganglion cells, astrocyte, astrocytes, astrogliosis, autoimmune encephalomyelitis, demyelination, human, inflammatory demyelinating disease of the central nervous system, mice, mouse, neurodegeneration, neuroinflammation, optic neuritis, patient, people, retinal degeneration, retinal ganglion cell, retinal neurodegeneration, tdTomato
Author NameAffiliation
Donald J ZackWilmer Eye Institute, Johns Hopkins University School of Medicine
Donald J ZackJohns Hopkins University
Donald J ZackThe Guerrieri Center for Genetic Engineering and Molecular Ophthalmology, The Wilmer Eye Institute, The Johns Hopkins University School of Medicine
Charles G EberhartWilmer Eye Institute, Johns Hopkins University School of Medicine
Charles G EberhartThe Johns Hopkins University School of Medicine
Charles G EberhartWilmer Eye Institute, Johns Hopkins University School of Medicine
Charles G EberhartThe Johns Hopkins University School of Medicine
Peter A CalabresiJohns Hopkins Hospital
Peter A CalabresiJohns Hopkins University
Peter A CalabresiWilmer Eye Institute, Johns Hopkins University School of Medicine
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Release 1.2