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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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Innate Immune Reprogramming Mediated by Endogenous Retroelement Dysregulation Drives Multiple Sclerosis Progression.

Li-Mei Xiao1,2,3, Qiu-Ping Zhao1,2,3, Run-Yun Li1,3

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

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Summary
This summary is machine-generated.

A shared H3.3 low/endogenous retroelements (EREs) high signature in bone marrow myelopoiesis links multiple sclerosis (MS) and post-COVID-19 conditions, offering new therapeutic insights for MS progression.

Keywords:
H3.3MSendogenous retroelementsmyelopoiesisneuroinflammation

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Area of Science:

  • Immunology
  • Genetics
  • Neurology

Background:

  • Skewed myelopoiesis is a key driver of multiple sclerosis (MS) progression.
  • SARS-CoV-2 infection can induce myelopoiesis similar to that seen in MS.
  • Dysregulation of endogenous retroelements (EREs) in hematopoietic stem and progenitor cells (HSPCs) can cause skewed myelopoiesis.

Purpose of the Study:

  • To investigate if ERE dysregulation contributes to skewed myelopoiesis in MS and post-COVID-19.
  • To identify common mechanisms underlying skewed myelopoiesis in both conditions.

Main Methods:

  • Joint analysis of two public single-cell/nuclei cohorts (MS and post-COVID-19).
  • Application of an identical bioinformatic pipeline for gene and ERE expression assessment.

Main Results:

  • Enhanced myelopoiesis observed in MS patients compared to controls.
  • Downregulation of the ERE repressor H3.3 and overexpression of EREs found in MS.
  • Similar epigenetic and transcript features identified in post-COVID-19 individuals.

Conclusions:

  • The H3.3 low/ERE high signature may explain common skewed myelopoiesis in MS and post-COVID-19.
  • This signature provides a mechanistic link between infection and innate immune reprogramming in MS.
  • Offers novel therapeutic insights for MS progression.