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Related Concept Videos

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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.
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The stem cell niche is the dynamic microenvironment where stem cells reside. Inside these niches, the cells may remain undifferentiated, undergo high self-renewal, or become lineage-specific progenitors. Stem cells coexist with other niche cells, such as stromal cells. They also interact closely with the ECM. Cell-cell and cell-matrix communication occur via adhesion molecules or soluble factors that signal the stem cells and determine their fate. Stromal cells also provide survival signals to...
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Related Experiment Video

Updated: Jan 12, 2026

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
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Single-cell spatial transcriptomic profiling defines a pathogenic inflammatory niche in chronic active multiple

Ruoqing Feng1, Lena Spieth1, Lu Liu1

  • 1Institute of Neuronal Cell Biology, Technical University Munich, Munich, Germany; German Center for Neurodegenerative Diseases, Munich, Germany.

Immunity
|October 30, 2025
PubMed
Summary

Researchers mapped immune cells in active multiple sclerosis (MS) lesions, revealing lipid-metabolizing microglia drive persistent neuroinflammation. Targeting lipid metabolism reduced inflammation and demyelination in mouse models, offering new therapeutic avenues for MS.

Keywords:
CD8+ T cellsCD8+ tissue-resident memory T cellsglialipidsmicrogliamultiple sclerosismyelinneuroinflammationspatial transcriptomics

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Area of Science:

  • Neuroimmunology
  • Cellular and Molecular Neuroscience

Background:

  • Compartmentalized inflammation drives multiple sclerosis (MS) progression.
  • The mechanisms behind persistent inflammation in chronic active MS lesions are not fully understood.

Purpose of the Study:

  • To create a high-resolution spatial and molecular atlas of immune niches within chronic active MS lesions.
  • To elucidate the role of specific immune cell interactions and metabolic pathways in sustaining neuroinflammation in MS.

Main Methods:

  • Combined single-nucleus RNA sequencing (snRNA-seq) with multiplexed error-robust fluorescence in situ hybridization (MERFISH) to map cellular and molecular features of MS lesions.
  • Utilized mouse models of experimental autoimmune encephalomyelitis (EAE) to investigate the function of microglia and lipid metabolism.
  • Genetically deleted ATP-binding cassette transporters ABCA1/G1 in microglia and pharmacologically targeted sterol metabolism.

Main Results:

  • Identified CD8+ T cell niches in lesion rims associated with inflamed microglia exhibiting interferon responses and altered lipid metabolism.
  • Deleting ABCA1/G1 in microglia led to increased lipid-storing phagocytes and amplified inflammation in EAE mice.
  • Pharmacological inhibition of sterol metabolism reduced foam cell formation and inflammatory demyelination in EAE models.

Conclusions:

  • Dysfunctional, lipid-storing microglia contribute to persistent neuroinflammation in chronic active MS lesions.
  • Targeting microglial lipid metabolism presents a potential therapeutic strategy for mitigating inflammation and demyelination in multiple sclerosis.