Meningeal B-cell follicles in secondary progressive multiple sclerosis associate with early onset of disease and severe cortical pathology.

By R. Magliozzi, O. Howell, A. Vora, B. Serafini, R. Nicholas, M. Puopolo, R. Reynolds, F. Aloisi. Brain : a journal of neurology, 2007

1,431 citations recorded by the source corpus.

Subfields: Immunology, Neurology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/82b25397c22b1d7c620f95eb7387f52eb7c19bbc

How researchers see this paper

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

In Immunology

1. Hans Lassmann
2. Roland Martin
3. F. Aloisi
4. J. Buckner
5. C. Iadecola
6. J. Goverman
7. R. Ransohoff

In Neurology

1. Hans Lassmann
2. C. Lucchinetti

In Pathology and Forensic Medicine

1. Hans Lassmann
2. C. Lucchinetti
3. Roland Martin
4. F. Aloisi
5. C. Iadecola
6. J. Buckner
7. R. Ransohoff

Citations in the corpus

• Pathogenic Mechanisms Associated With Different Clinical Courses of Multiple Sclerosis (2019, background): “Evidence from expanding cortical lesions and slowly expanding white matter lesions suggest that demyelination and neurodegeneration is driven by an MS specific soluble factor, produced by inflammatory cells, which induces tissue damage either directly or indirectly through microglia activation (83),”
• Innate immunity in the central nervous system. (2012, neutral): “Because neutrophils also promote B cell survival and proliferation (120), innate neutrophils and mast cells might contribute to the B cell follicle–like structures that are found at autopsy in the meninges of MS tissues (134, 135).”
• The relation between inflammation and neurodegeneration in multiple sclerosis brains (2009, background): “The above mentioned studies do not exclude the possibility that a diffuse inflammatory process in inactive lesions, the NAWM, the cortex or the meninges may ultimately drive neurodegeneration at these sites (Kornek et al., 2000; Kutzelnigg et al., 2005; Magliozzi et al., 2007).”
• Multiple Sclerosis Pathology. (2018, background): “Such inflammatory follicle-like structures in themeninges are associated with particularly severe active demyelination in the underlying cortex (Magliozzi et al. 2007).”
• Meningeal inflammation is widespread and linked to cortical pathology in multiple sclerosis. (2011, methodology): “, 2003a, b), precludes a role for perivascular inflammation and suggests that an immune response in the inflamed meninges might play a role in the pathogenesis of the underlying grey matter pathology (Peterson et al., 2001; Kutzelnigg et al., 2005; Magliozzi et al., 2007; Dal Bianco et al., 2008).”
• Multiple sclerosis: a complicated picture of autoimmunity (2007, background): “One of the characteristic clinical findings is an increase in intrathecally synthesized immunoglobulin G in the cerebrospinal fluid of patients, reflecting retention of clonal populations of B cells in the nervous system or meningeal B cell follicle”