What question did this study set out to answer?

To identify the pathogenic role and regulatory mechanisms of GM-CSF-producing B cell subsets in multiple sclerosis and determine how B cell depletion therapy impacts their function.

October 21, 2015Science Translational Medicine

Proinflammatory GM-CSF–producing B cells in multiple sclerosis and B cell depletion therapy

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Authors

RLRui LiFujian University of Traditional Chinese Medicine ARAyman RezkUniversity of Pennsylvania YMYusei MiyazakiNational Hospital Organization Hokkaido Medical Center

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Overview

Mechanistic study reveals elevated GM-CSF-producing B cells activate myeloid cells in multiple sclerosis, indicating that B cell depletion therapy restores cytokine balance to curb inflammation.

Key Points

To identify the pathogenic role and regulatory mechanisms of GM-CSF-producing B cell subsets in multiple sclerosis and determine how B cell depletion therapy impacts their function.
Analyzed frequency and in vitro induction of GM-CSF-expressing memory B cells from multiple sclerosis patients compared with healthy controls.
Assessed myeloid cell activation in vitro and profiled proinflammatory myeloid responses in vivo before and after B cell depletion therapy.
Investigated the role of STAT5 and STAT6 signaling in regulating the balance between GM-CSF and IL-10 cytokine production during B cell reconstitution.
Memory B cells expressing GM-CSF were significantly more frequent in patients with multiple sclerosis and activated myeloid cells in a GM-CSF-dependent manner.
Enhanced STAT5 and STAT6 signaling in untreated patients drove GM-CSF production while reciprocally suppressing regulatory IL-10 expression in B cells.
B cell depletion therapy normalized STAT5/6 signaling and the GM-CSF/IL-10 secretion ratio, maintaining reduced proinflammatory myeloid responses even after B cell repopulation.

Cite This Study

Li et al. (2015) studied this question.

synapsesocial.com/papers/6a7ccea9469490254d190c8f https://doi.org/10.1126/scitranslmed.aab4176

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October 21, 2015Science Translational Medicine

Proinflammatory GM-CSF–producing B cells in multiple sclerosis and B cell depletion therapy

View Full Paper

Ask AI

Bookmark

Authors

RLRui LiFujian University of Traditional Chinese Medicine ARAyman RezkUniversity of Pennsylvania YMYusei MiyazakiNational Hospital Organization Hokkaido Medical Center

Discussion

Member takes

Overview

Mechanistic study reveals elevated GM-CSF-producing B cells activate myeloid cells in multiple sclerosis, indicating that B cell depletion therapy restores cytokine balance to curb inflammation.

Key Points

To identify the pathogenic role and regulatory mechanisms of GM-CSF-producing B cell subsets in multiple sclerosis and determine how B cell depletion therapy impacts their function.
Analyzed frequency and in vitro induction of GM-CSF-expressing memory B cells from multiple sclerosis patients compared with healthy controls.
Assessed myeloid cell activation in vitro and profiled proinflammatory myeloid responses in vivo before and after B cell depletion therapy.
Investigated the role of STAT5 and STAT6 signaling in regulating the balance between GM-CSF and IL-10 cytokine production during B cell reconstitution.
Memory B cells expressing GM-CSF were significantly more frequent in patients with multiple sclerosis and activated myeloid cells in a GM-CSF-dependent manner.
Enhanced STAT5 and STAT6 signaling in untreated patients drove GM-CSF production while reciprocally suppressing regulatory IL-10 expression in B cells.
B cell depletion therapy normalized STAT5/6 signaling and the GM-CSF/IL-10 secretion ratio, maintaining reduced proinflammatory myeloid responses even after B cell repopulation.

Cite This Study

Li et al. (2015) studied this question.

synapsesocial.com/papers/6a7ccea9469490254d190c8f https://doi.org/10.1126/scitranslmed.aab4176

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