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Progressive Multiple Sclerosis Transcriptome Deconvolution Indicates Increased M2 Macrophages in Inactive Lesions.

Sai Batchu1

  • 1National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda, Maryland, USA, batchus1@tcnj.edu.

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M2 macrophages, crucial for tissue repair in multiple sclerosis (MS), were found in higher numbers in inactive MS lesions. This suggests a potential role for these immune cells in managing disease activity.

Keywords:
LesionMacrophageMultiple sclerosisRNA-Sequencing

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Area of Science:

  • Neuroimmunology
  • Immunology
  • Pathology

Background:

  • M2 macrophages are implicated in tissue repair and inflammation control in multiple sclerosis (MS).
  • Previous research primarily utilized murine models, lacking direct human MS patient data.
  • Understanding M2 macrophage roles in human MS lesions is critical for therapeutic development.

Purpose of the Study:

  • To quantify M2 macrophage abundance in distinct human MS lesion types.
  • To correlate M2 macrophage levels with lesion activity status in progressive MS.
  • To provide human-based evidence for M2 macrophage function in MS pathology.

Main Methods:

  • Analysis of bulk RNA-sequencing data from 98 lesions of 10 progressive MS patients and 5 controls.
  • Application of the CIBERSORTx RNA deconvolution algorithm.
  • Utilized a validated gene signature matrix for 22 human hematopoietic cell subsets.

Main Results:

  • Inactive MS lesions exhibited significantly higher relative abundances of M2 macrophages compared to normal white matter.
  • M2 macrophage proportions varied across different lesion types within MS patients.
  • The findings provide quantitative data on M2 macrophage presence in human MS lesions.

Conclusions:

  • M2 macrophages are significantly enriched in inactive lesions of multiple sclerosis.
  • These findings support a role for M2 macrophages in the resolution or inactivity phase of MS lesions.
  • Further investigation into M2 macrophage-targeted therapies for MS is warranted.