Compartmentalization of inflammation in the CNS: A major mechanism driving progressive multiple sclerosis

  title={Compartmentalization of inflammation in the CNS: A major mechanism driving progressive multiple sclerosis},
  author={Edgar Meinl and Markus Krumbholz and Tobias Derfuss and Andreas Junker and Reinhard Hohlfeld},
  journal={Journal of the Neurological Sciences},

Inflammatory mechanisms underlying cortical injury in progressive multiple sclerosis

A better understanding of the interplay between peripheral immune and CNS resident cells is not only relevant to the concept of the disease process, but also represents a novel target for therapeutic intervention that is more specific to progressive disease biology.

Intrathecal immune reset in multiple sclerosis: exploring a new concept.

The neuropathological basis of clinical progression in multiple sclerosis

The contributions that the various types of pathology are likely to make to the increasing neurological deficit in MS are reviewed.

Role of B cells and antibodies in multiple sclerosis.

Multiple sclerosis animal models: a clinical and histopathological perspective

To what extent pathology of the progressive disease stage can be modeled in MS animal models is discussed, and which pathological aspects of the disease can be best studied in the various animal models available is discussed.

Past, Present and Future of Cell-Based Therapy in Progressive Multiple Sclerosis

Major expectation arises from the use of oligodendrocyte progenitor cells for directly replacing the damaged myelin and non-haematopoietic stem cells for the potential of influencing host immune response and endogenous mechanisms of repair.

Intense Inflammation and Nerve Damage in Early Multiple Sclerosis Subsides at Older Age: A Reflection by Cerebrospinal Fluid Biomarkers

A strong effect of age on both inflammatory and neurodegenerative biomarkers in a large cohort of MS patients is demonstrated and may provide a biological explanation for the relative inefficacy of such treatments in older patients at later disease stages.

The relation between inflammation and neurodegeneration in multiple sclerosis brains

It is found that pronounced inflammation in the brain is not only present in acute and relapsing multiple sclerosis but also in the secondary and primary progressive disease, and the disease processes of multiple sclerosis may die out in aged patients with long-standing disease.

Intrathecal rituximab therapy in multiple sclerosis: review of evidence supporting the need for future trials.

The recent evidence supporting the need for trials based on the intrathecal use of rituximab in multiple sclerosis is summarized.



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

Data support an immunopathogenetic mechanism whereby B-cell follicles developing in the multiple sclerosis meninges exacerbate the detrimental effects of humoral immunity with a subsequent major impact on the integrity of the cortical structures.

Identification of a pathogenic antibody response to native myelin oligodendrocyte glycoprotein in multiple sclerosis

Overall these findings suggest a pathogenic antibody response to native MOG in a subgroup of MS patients, and its implication for demyelination and axonal loss in MS.

Short-lived plasma blasts are the main B cell effector subset during the course of multiple sclerosis

This study identifies short-lived plasma blasts as the main effector B cell population involved in ongoing active inflammation in multiple sclerosis patients.

B lineage cells in the inflammatory central nervous system environment: Migration, maintenance, local antibody production, and therapeutic modulation

These new findings offer a plausible explanation for the notorious persistence and stability of cerebrospinal fluid oligoclonal bands and outline the possibly double‐edged effects of B cells and immunoglobulin in the CNS.

Neurofascin as a novel target for autoantibody-mediated axonal injury

A novel mechanism of immune-mediated axonal injury that can contribute to axonal pathology in MS is identified and identified through a proteomics-based approach.

Detection of Ectopic B‐cell Follicles with Germinal Centers in the Meninges of Patients with Secondary Progressive Multiple Sclerosis

Lymphoid follicle‐like structures containing B‐cells, T‐cells and plasma cells, and a network of follicular dendritic cells producing CXCL13 were observed in the cerebral meninges of 2 out of 3 patients with secondary progressive MS, but not in relapsing remitting and primary progressive MS.

Dysregulated Epstein-Barr virus infection in the multiple sclerosis brain

Findings from this study are interpreted as evidence that EBV persistence and reactivation in the CNS play an important role in MS immunopathology.

Persistent endothelial abnormalities and blood–brain barrier leak in primary and secondary progressive multiple sclerosis

Epithelial and endothelial tight junctions are pathologically altered in infectious, inflammatory, neoplastic and other diseases. Previously, we described such abnormalities, associated with serum

Multiple sclerosis: T-cell receptor expression in distinct brain regions.

P pervasive T-cell clones exist in distinct regions of MS brain, and these clones are 'private' (unique) to individual patients, supporting the pathogenic relevance of this T- cell subset.