Enhanced costimulation by CD70+ B cells aggravates experimental autoimmune encephalomyelitis in autoimmune mice

FrancoSalinas, Gabriela; Cantaert, Tineke; Nolte, Martijn A.; Tak, Paul P.; Lier, R. A. W. Van; Baeten, Dominique

doi:10.1016/j.jneuroim.2012.10.010

Cited by 14 publications

(17 citation statements)

References 78 publications

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“…Interestingly, anti-CD70 antibody-mediated blocking of CD70 prevented EAE in SJL/J mice (121), and over-expression of CD70 on the B cells enhanced EAE (126). This is in contrast to what is reported by Coquet et al (124).…”

Section: Cd70-cd27mentioning

confidence: 59%

“…Differential entry sites into the CNS likely contribute to location specificity. Expression of CCL20 (a CCR6 ligand) by epithelial cells of the choroid plexus appear to promote CCR6-regulated entry of Th17 cells (126). Whether anatomical differences in the tissue structure or ECM composition at these locations impacts the efficiency of Th1 or Th17 migration is not yet clear.…”

Section: Unique Lanscape Of the Cnsmentioning

confidence: 99%

“…At disease onset, or during relapses, proinflammatory monocytes migrate to the CNS, where their numbers directly correlate with the severity of EAE symptoms (124)(125)(126) and in turn, with elevated levels of neurotoxic QUIN in the spinal cord (67). This migration might be facilitated by a damaged BBB, one of the earliest clinical findings in MS, thought to play a fundamental role in the development of the disease [see BBB Breakdown and Entry of Immune Cells as a Key Hallmark of Early MS Pathology; Ref.…”

Section: Peripheral Blood Monocytes As a Potent Source Of Inflammatormentioning

confidence: 99%

“…(86,87)]. To confirm that monocyte migration to the CNS is involved in EAE pathogenesis, Mishra and colleagues have demonstrated that its inhibition by the candidate MS drug Laquinimod prevented the onset of EAE and its clinical signs (126). More recently, depletion of phagocytotic monocytes by clodronate treatment reduced the severity of EAE symptoms and protected against further axonal loss (127).…”

Section: Peripheral Blood Monocytes As a Potent Source Of Inflammatormentioning

confidence: 99%

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Inflammation in the CNS: Advancing the Field Using Intravital Imaging

Pai¹,

Hickey²,

Weninger³

2017

Frontiers Research Topics

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Section: Cd70-cd27mentioning

confidence: 59%

Section: Unique Lanscape Of the Cnsmentioning

confidence: 99%

Section: Peripheral Blood Monocytes As a Potent Source Of Inflammatormentioning

confidence: 99%

Section: Peripheral Blood Monocytes As a Potent Source Of Inflammatormentioning

confidence: 99%

See 2 more Smart Citations

Inflammation in the CNS: Advancing the Field Using Intravital Imaging

Pai¹,

Hickey²,

Weninger³

2017

Frontiers Research Topics

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“…Coquet et al [20] found that the CD27-CD70 costimulatory pathway impeded Th17 cell differentiation and associated autoimmunity in experimental autoimmune encephalomyelitis (EAE) by selectively repressing the transcription of IL-17 and CCR6 [21]. However, other studies found that CD27-CD70 signal-blocking prevented EAE in SJL/J mice [22] and the overexpression of CD70 in B cells enhanced EAE in 2D2 mice [23]. Although the role of CD27-CD70 in Th17 regulation is inconsistent, maybe due to the pleiotropic and complex effects of CD70-CD27 interaction on T cell and B cell activation [9, 10], CD27-CD70 is sure to be one of the components of the Th17 pathway.…”

Section: Discussionmentioning

confidence: 99%

Cerebrospinal Fluid Level of Soluble CD27 Is Associated with Disease Severity in Neuromyelitis Optica Spectrum Disorder

Liu¹,

Zhong²,

Liu³

et al. 2018

Neuroimmunomodulation

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Object: CD27 belongs to the tumor necrosis factor receptor family and is constitutively expressed on T cells. The concentration of cerebrospinal fluid (CSF) soluble (s)CD27 is elevated in patients with multiple sclerosis (MS). However, whether the level of CSF sCD27 is elevated in neuromyelitis optica spectrum disorder (NMOSD) remains unknown. The aim of this study was to measure the CSF concentration of sCD27 and to determine its relationship with NMOSD disease activity. Methods: CSF CXCL13 was measured by ELISA in neuromyelitis optica (NMO) (n = 31) and MS (n = 23) patients and in controls (CTLs) (n = 22). Results: The concentration of sCD27 was higher in the NMO group than in the MS (p = 0.082) and CTL (p = 0.002) groups, and there was a positive correlation with CSF IL-6 (p = 0.000) and a negative correlation with IL-10 (p = 0.073). In the NMO group, patients with higher sCD27 concentrations exhibited worse disease disability in their CSF (p = 0.006). Moreover, the sCD27 concentrations had a significantly positive correlation with the level of CSF total protein (p = 0.030). Furthermore, the patients positive for AQP4-IgG (n = 26) seemed to have higher levels of sCD27 in their CSF (p = 0.069) than those negative for AQP4-IgG (n = 5). Conclusions: We revealed that the level of CSF sCD27 was elevated in NMOSD and correlated with NMOSD disease activity.

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Effects of Glatiramer Acetate in a Spontaneous Model of Autoimmune Neuroinflammation

Bittner

Ruck

Göbel

et al. 2014

The American Journal of Pathology

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Glatiramer acetate (GA) (Copaxone), a well-established drug for the treatment of multiple sclerosis, is believed to modulate numerous pathways including antigen-presenting cells or cytokine responses. A new generation of spontaneous experimental autoimmune encephalomyelitis mouse models has been developed that mimic certain aspects of multiple sclerosis spectrum disorders. We assessed the effects of GA in the opticospinal encephalomyelitis model, which involves MOG35-55 peptide-specific T cells and B cells. A nonsignificant trend toward lower disease incidence was found for GA treatment (started on postnatal day 20). Immunohistochemical evaluations revealed no significant differences for inflammatory lesions and demyelination, cytokine production, proliferation, and cell surface markers of immune cells between GA-treated and PBS-treated (control) mice. Although a good correlation was found between the disease score of individual mice and some readout parameters (eg, immunohistochemical staining), this was not the case for others (eg, IFN-γ production). It seems plausible that a major effect of GA lies on alternative immunological pathways, such as initiating of an immune response that is not sufficiently reflected in this spontaneous experimental autoimmune encephalomyelitis model. Thus, the main advantage of the opticospinal encephalomyelitis model in our hands lies in the elucidation of factors influencing the onset of experimental autoimmune encephalomyelitis (eg, susceptibility factors). The model seems less suitable for investigation of disease severity modifications after therapeutic interventions.

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Enhanced costimulation by CD70+ B cells aggravates experimental autoimmune encephalomyelitis in autoimmune mice

Abstract: Expression of CD70 by B cells aggravates EAE possibly by reducing the number of regulatory T cells.

Cited by 14 publications

References 78 publications

Inflammation in the CNS: Advancing the Field Using Intravital Imaging

Inflammation in the CNS: Advancing the Field Using Intravital Imaging

Cerebrospinal Fluid Level of Soluble CD27 Is Associated with Disease Severity in Neuromyelitis Optica Spectrum Disorder

Effects of Glatiramer Acetate in a Spontaneous Model of Autoimmune Neuroinflammation

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