Abnormal B‐cell cytokine responses a trigger of T‐cell–mediated disease in MS?

Bar‐Or, Amit; Fawaz, Lama; Fan, Baochao; Darlington, Peter J.; Rieger, Aja M.; Ghorayeb, Christine; Calabresi, Peter A.; Waubant, Emmanuelle; Hauser, Stephen L.; Zhang, Jiameng; Smith, Craig H.

doi:10.1002/ana.21939

Cited by 461 publications

(456 citation statements)

References 44 publications

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“…Several studies have shown that the B cells of patients with MS have defects in the balance of their cytokine expression, with a propensity for overproduction of inflammatory cytokines [e.g., lymphotoxin, tumor necrosis factor alpha (TNF-α), interleukin (IL)-6] and a deficit in production of anti-inflammatory cytokines (e.g., IL-10) [91][92][93]. In studies of patients with MS who underwent B-cell depletion, treatment resulted in Fig.…”

Section: B-cell Cytokines and B-cell/t-cell Interactions In Msmentioning

confidence: 99%

Neuroinflammation: Ways in Which the Immune System Affects the Brain

et al. 2015

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Neuroinflammation is the response of the central nervous system (CNS) to disturbed homeostasis and typifies all neurological diseases. The main reactive components of the CNS include microglial cells and infiltrating myeloid cells, astrocytes, oligodendrocytes, and the blood-brain b a r r i e r , c y t o k i n e s , a n d c y t o k i n e s i g n a l i n g . Neuroinflammatory responses may be helpful or harmful, as mechanisms associated with neuroinflammation are involved in normal brain development, as well as in neuropathological processes. This review examines the roles of various cell types that contribute to the immune dysregulation associated with neuroinflammation. Microglia enter the CNS very early in embryonic development and, as such, play an essential role in both the healthy and diseased brain. B-cell diversity contributes to CNS disease through both antibody-dependent and antibody-independent mechanisms. The influences of these B-cell mechanisms on other cell types, including myeloid cells and T cells, are reviewed in relationship to antibody-mediated CNS disorders, paraneoplastic neurological diseases, and multiple sclerosis. New insights into neuroinflammation offer exciting opportunities to investigate potential therapeutic targets for debilitating CNS diseases.

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Section: B-cell Cytokines and B-cell/t-cell Interactions In Msmentioning

confidence: 99%

Neuroinflammation: Ways in Which the Immune System Affects the Brain

et al. 2015

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“…Recent evidence suggests that a subset of B cells has an active role in the etiology of MS and may potentiate activity of MS-promoting T cells [34]. Reports that administration of antibody Rituximab, which targets CD20 on B cells, is effective at treating MS corroborate this hypothesis [34,35].…”

Section: Ahsct Mechanism Of Action: the Immunosuppression Hypothesismentioning

confidence: 93%

“…Reports that administration of antibody Rituximab, which targets CD20 on B cells, is effective at treating MS corroborate this hypothesis [34,35]. Interestingly, alemtuzumab also substantially affects B-cell homeostasis, and the reconstitution of these cells contrasts dramatically with that of the T cells [36].…”

Section: Ahsct Mechanism Of Action: the Immunosuppression Hypothesismentioning

confidence: 94%

Immune Mechanisms Underlying the Beneficial Effects of Autologous Hematopoietic Stem Cell Transplantation in Multiple Sclerosis

Gosselin

Rivest

2011

Neurotherapeutics

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A recent phase I/II clinical trial drew serious attention to the therapeutic potential of autologous hematopoietic stem cell transplantation (AHSCT) in multiple sclerosis. However, questions were raised as to whether these beneficial effects should be attributed to the newly reconstituted immune system per se, or to the lymphoablative conditioning regimeninduced immunosuppression, given that T-cell depleting combinational drug therapies were used in the study. We discuss here the possibility that both AHSCT and T-cell depleting therapies may re-program alternatively the immune system, and why transplantation of CD34 + hematopoietic stem cells may offer AHSCT a possible advantage regarding longterm remission.

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“…[15] Rituksimab, anti-CD20 monoklonal antikordur, dolaşımdaki B hücrelerini tüketir, bunun sonuçu olarak, CD4+ ve CD8+ T hücre yanıtlarını etkiler, bir olguda nöbet kontrolünde etkili olduğu bildirilmiştir. [16] Son zamanlarda bazı RE'li hastalarda veya ailerinde ikinci bir otoimmün hastalık görüldüğü bildirilmiştir. RE ve Behçet hastalığının birinci derece akrabalarda görülmesi, RE'nin diğer otoimmün hastalıklarla genetik bir yatkınlık paylaştığını düşündürmüştür.…”

Section: Introductionunclassified

Epileptic Syndromes With Possible Immunological Mechanisms (Rasmussen Encephalitis, FIRES, West Syndrome, Landau-Kleffner Syndrome)

Kınay¹

2015

Epilepsi

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SummarySome of childhood epileptic syndromes reminds immunological etiologies with their good response to immuno-therapy and histopathological findings. These syndromes, such as Rasmussen encephalitis, FIRES, West syndrome, and Landau-Kleffner syndrome each of which are proceeding with severe epileptic encephalopathy are discussed with their physiopathological, clinical, EEG, laboratory, treatment and prognostic characteristics by the help of current literatüre.

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Abnormal B‐cell cytokine responses a trigger of T‐cell–mediated disease in MS?

Cited by 461 publications

References 44 publications

Neuroinflammation: Ways in Which the Immune System Affects the Brain

Neuroinflammation: Ways in Which the Immune System Affects the Brain

Immune Mechanisms Underlying the Beneficial Effects of Autologous Hematopoietic Stem Cell Transplantation in Multiple Sclerosis

Epileptic Syndromes With Possible Immunological Mechanisms (Rasmussen Encephalitis, FIRES, West Syndrome, Landau-Kleffner Syndrome)

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