Heterogeneity of multiple sclerosis lesions: Implications for the pathogenesis of demyelination
By C. Lucchinetti, Wolfgang Brück, Joseph E. Parisi, B. Scheithauer, Moses Rodriguez, Hans Lassmann. Annals of Neurology, 2000
3,423 citations recorded by the source corpus.
Subfields: Neurology, Pathology and Forensic Medicine, Rheumatology
View Paper: https://www.semanticscholar.org/paper/cfb7afc49b92e90473f197a6f30177a126bd1803
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Neurology
- Hans Lassmann
- C. Lucchinetti
- J. Goverman
- Wolfgang Brück
- R. Ransohoff
- B. Weinshenker
- Sandra Vukusic
- C. ffrench-Constant
In Pathology and Forensic Medicine
- Hans Lassmann
- C. Lucchinetti
- R. Ransohoff
- Wolfgang Brück
- B. Weinshenker
- Sandra Vukusic
- Christian Confavreux
- D. Wingerchuk
In Rheumatology
Citations in the corpus
- Meningeal B-cell follicles in secondary progressive multiple sclerosis associate with early onset of disease and severe cortical pathology. (2007, background): “Neuropathological studies indicate that antibodymediated demyelination is one of the predominant pathogenetic mechanisms involved in white matter lesion formation in a substantial proportion of multiple sclerosis patients (Lucchinetti et al., 2000).”
- CNS immune privilege: hiding in plain sight (2006, background): “In support of this view, T cells are found in perivascular cuffs and within the demyelinated lesions in patients with multiple sclerosis (MS), an autoimmune demyelinating disorder (6, 13).”
- Grey Matter Pathology in Multiple Sclerosis (2005, background): “Heterogeneity of the pathogenic process in white matter demyelinating lesions in MS has been described (30); grey matter demyelination could also present a similar heterogeneity.”
- Multiple Sclerosis Pathology. (2018, background): “Based on knowledge from experimental models, there are many different immunological mechanisms that may be involved in this process, and the question arises, which of these mechanisms are relevant for MS (Lucchinetti et al. 2000; Lassmann et al. 2012).”
- Natural history of multiple sclerosis: a unifying concept. (2006, background): “For some of them, the term of multiple sclerosis could even encompass separate disease entities (Lucchinetti et al., 2000; Weinshenker, 2000).”
- Autoimmune T cell responses in the central nervous system (2009, background): “This suggests that many pathways involving distinct effector mechanisms can lead to chronic autoimmune disease in the CN”
- An updated histological classification system for multiple sclerosis lesions (2016, methodology): “Lucchinetti and colleagues subdivided active and early demyelinating lesions further into four different histological patterns (pattern I, II, III, IV) [33].”
- Understanding pathogenesis and therapy of multiple sclerosis via animal models: 70 years of merits and culprits in experimental autoimmune encephalomyelitis research. (2006, background): “…generation of myelin-specific antibodies by B lymphocytes, and the same mechanism appears to be involved in the pathogenesis of lesion formation in both a subset of multiple sclerosis patients (Lucchinetti et al., 2000) and patients with Devic's type of neuromyelitis optica (Lennon et al., 2004).”
- Relapsing and remitting multiple sclerosis: Pathology of the newly forming lesion (2004, background): “In previous studies in which partly myelinated lesions resembling those described here have been examined, it has been noted that no similar lesions are known to occur in any experimental model involving T cell– or antibody-mediated immunity directed against an oligodendrocyte or myelin antigen.(23,”