Experimental autoimmune encephalomyelitis repressed by microglial paralysis

By Frank Heppner, M. Greter, D. Marino, J. Falsig, G. Raivich, N. Hövelmeyer, A. Waisman, T. Rülicke, Marco Prinz, Josef Priller and 2 more. Nature Medicine, 2005

775 citations recorded by the source corpus.

Subfields: Immunology, Neurology

View Paper: https://www.semanticscholar.org/paper/0bfa1d39bb7192eb8f2938b34177e410ae794b7b

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Citations in the corpus

Microglial physiology: unique stimuli, specialized responses. (2009, background): “MS research has depended largely on an autoimmune animal model, EAE, that exhibits features of CNS inflammatory demyelination and paralysis that resemble aspects of MS.”
Infiltrating monocytes trigger EAE progression, but do not contribute to the resident microglia pool (2011, methodology): “Experiments using bone marrow chimeras suggest that the activation of resident microglia may represent one of the initial steps in EAE pathogenesis, preceding and possibly triggering the infiltration of blood-derived cell”
Single-cell profiling identifies myeloid cell subsets with distinct fates during neuroinflammation (2019, background): “These suggested major roles of microglia, including the expression of proinflammatory mediators and effector molecules at the peak of disease (30, 60) and the removal of debris, which allows proper remyelination during the recovery phase (49, 61).”
Innate immunity and neuroinflammation in the CNS: The role of microglia in Toll‐like receptor‐mediated neuronal injury (2009, background): “Inhibition of microglial activity protects the brain from inflammatory lesions (Heppner et al., 2005).”
Protein aggregation diseases: pathogenicity and therapeutic perspectives (2010, background): “However, depletion of microglia led to a nearly 15-fold increase in prion infectivity in a slice culture model of prion diseas”
Understanding pathogenesis and therapy of multiple sclerosis via animal models: 70 years of merits and culprits in experimental autoimmune encephalomyelitis research. (2006, background): “…for mediating this pathology, as macrophages are the dominant effector cell population responsible for acute clinical disease in EAE: the number of macrophages infiltrating the CNS correlates broadly with disease severity (Berger et al., 1997; McQualter et al., 2001; Heppner et al., 2005).”
Microglia: active sensor and versatile effector cells in the normal and pathologic brain (2007, background): “In a complex mouse model of a demyelinating disorder in which microglial activation is reduced, disease development is attenuated [ 62 ].”
Essential protective roles of reactive astrocytes in traumatic brain injury. (2006, background): “…an overall harmful effect; otherwise an improved response might have been expected in a manner similar to the improved response to experimental autoimmune encephalomyelitis that was observed when microglia were ablated using transgenically targeted HSV-TK and ganciclovir (Heppner et al., 2005).”
Innate immunity in the central nervous system. (2012, positive): “In transgenic mice, EAE was less severe if microglial responses were impaired (116).”
The myeloid cells of the central nervous system parenchyma (2010, background): “Involvement of the parenchymal microglia seems limited to an undefined role in worsening disease severity, as has been shown in animals with experimental autoimmune encephalomyelitis, a model of immune-mediated brain inflammatio”