A role for humoral mechanisms in the pathogenesis of Devic's neuromyelitis optica.

By C. Lucchinetti, R. Mandler, D. McGavern, W. Bruck, G. Gleich, R. Ransohoff, C. Trebst, B. Weinshenker, D. Wingerchuk, Joseph E. Parisi and 1 more. Brain : a journal of neurology, 2002

1,208 citations recorded by the source corpus.

Subfields: Neurology, Pathology and Forensic Medicine, Rheumatology

View Paper: https://www.semanticscholar.org/paper/049a29fec3e6a3586c80fd66de8a3506adecfe01

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Neurology

1. Hans Lassmann
2. C. Lucchinetti
3. Wolfgang Brück
4. B. Weinshenker

In Pathology and Forensic Medicine

1. Hans Lassmann
2. C. Lucchinetti
3. Wolfgang Brück
4. B. Weinshenker
5. D. Wingerchuk
6. S. Pittock
7. V. Lennon

In Rheumatology

1. Hans Lassmann
2. C. Lucchinetti
3. Wolfgang Brück

Citations in the corpus

• Anti-aquaporin-4 antibody is involved in the pathogenesis of NMO: a study on antibody titre. (2007, background): “In the perivascular areas of those NMO lesions, immunoglobulins and activated complements were deposited (Lucchinetti et al., 2002; Misu et al., 2005b).”
• Pattern-specific loss of aquaporin-4 immunoreactivity distinguishes neuromyelitis optica from multiple sclerosis. (2007, background): “Deposits of IgG and IgM co-localize with products of complement activation in a vasculocentric pattern around thickened hyalinized blood vessels, suggesting a pathogenic role for humoral immunity targeting an antigen in the perivascular space (Lucchinetti et al., 2002).”
• Understanding pathogenesis and therapy of multiple sclerosis via animal models: 70 years of merits and culprits in experimental autoimmune encephalomyelitis research. (2006, background): “…(Weinshenker et al., 1999; Ruprecht et al., 2004) The clinical response to plasma exchange indicates the involvement of humoral immune mechanisms (Keegan et al., 2005), a concept supported by the extensive deposition of immunoglobulins and complement within the lesions (Lucchinetti et al., 2002).”
• Neuromyelitis optica and non organ-specific autoimmunity. (2008, background): “The target of NMO-IgG is AQP4, which occurs at the exact site of the deposition of immunoglobulins and products of complement activation in human NMO spinal cord lesions.(18) Furthermore, recent data reveal selective loss of AQP4 immunostaining in all NMO lesions, regardless of stage and despite pre”
• Neuromyelitis optica brain lesions localized at sites of high aquaporin 4 expression. (2006, result): “Downloaded From: by a Non-Human Traffic (NHT) User on 10/24/2018 et al1 for the diagnosis of NMO.”
• Loss of aquaporin 4 in lesions of neuromyelitis optica: distinction from multiple sclerosis. (2007, background): “…study on the distribution of AQP4, glial fibrillary acidic protein (GFAP), myelin basic protein (MBP), activated complement C9neo and immunoglobulins in the spinal cord lesions and medulla oblongata of NMO (n¼12), MS (n¼ 6), brain and spinal infarction (n¼ 7) and normal control (n¼ 8).”
• The Immunopathology of Multiple Sclerosis: An Overview (2007, background): “The pathology of Devic’s disease differs in several key aspects from that of classical MS (60).”