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Related Concept Videos

T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...

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Subsequent treatment strategies following rituximab-resistance in AQP4-IgG+ neuromyelitis optica spectrum disorder: a case series.

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Related Experiment Video

Updated: Jun 9, 2026

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4
09:29

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4

Published on: August 21, 2017

Synergistic Interaction Between MALAT1/miR-30b-5p/BAFF Axis and Inflammatory Cytokines Underlies Rituximab-Refractory

Meiqun Deng1,2, Keyi Zeng1,3, Wei Chen1,2,4

  • 1Department of Neurology, The First Affiliated Hospital, Fujian Medical University, Fuzhou, China.

CNS Neuroscience & Therapeutics
|June 8, 2026
PubMed
Summary

The MALAT1/miR-30b-5p/BAFF axis in monocytes drives neuromyelitis optica spectrum disorder (NMOSD) relapses, even after rituximab therapy. Targeting this pathway may prevent NMOSD relapses.

Keywords:
MALAT1/miR‐30b‐5p/BAFFmonocyteneuromyelitis optica spectrum disorderrituximab‐refractory

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Last Updated: Jun 9, 2026

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4
09:29

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Published on: August 21, 2017

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
07:09

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity

Published on: January 7, 2019

Area of Science:

  • Neuroimmunology
  • Molecular Biology
  • Genetics

Background:

  • Neuromyelitis optica spectrum disorder (NMOSD) patients can relapse despite B cell depletion with rituximab.
  • The mechanisms behind rituximab-refractory relapses in NMOSD are not fully understood.

Purpose of the Study:

  • To investigate the role of the MALAT1/miR-30b-5p/BAFF axis in monocytes in NMOSD pathogenesis.
  • To explore this axis's contribution to NMOSD relapses resistant to rituximab therapy.

Main Methods:

  • Quantified MALAT1, miR-30b-5p, BAFF, and cytokine levels in NMOSD patients and controls.
  • Utilized qPCR, ELISA, Western Blot, and dual-luciferase reporter assays.
  • Performed single-cell RNA sequencing and in vitro monocyte activation studies.

Main Results:

  • The MALAT1/miR-30b-5p/BAFF axis was activated in NMOSD patients at onset and correlated with rituximab-refractory relapse.
  • Monocyte-specific MALAT1 upregulation and elevated serum BAFF were observed in refractory relapse patients.
  • In vitro, MALAT1 overexpression downregulated miR-30b-5p, increasing BAFF and pro-inflammatory cytokines.

Conclusions:

  • The MALAT1/miR-30b-5p axis in monocytes drives NMOSD pathogenesis and rituximab-refractory relapse.
  • Monocytic MALAT1 upregulation suppresses miR-30b-5p, leading to increased BAFF and inflammatory cytokine secretion.
  • Targeting this axis presents a potential therapeutic strategy for NMOSD relapse prevention.