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Related Concept Videos

RNA-seq03:21

RNA-seq

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RNA sequencing, or RNA-Seq, is a high-throughput sequencing technology used to study the transcriptome of a cell. Transcriptomics helps to interpret the functional elements of a genome and identify the molecular constituents of an organism. Additionally, it also helps in understanding the development of an organism and the occurrence of diseases. 
Before the discovery of RNA-seq, microarray-based methods and Sanger sequencing were used for transcriptome analysis. However, while...
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Isolation of Region-specific Microglia from One Adult Mouse Brain Hemisphere for Deep Single-cell RNA Sequencing
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Single-Cell RNA Sequencing Uncovers Neutrophil Clusters Associated with Autoimmune Neuroinflammation.

Yong Wang1, William Turbitt1,2, Lianna Zhou1

  • 1University Blvd, University of Alabama at Birmingham, Birmingham, AL, USA 35294.

Research Square
|December 3, 2025
PubMed
Summary

Suppressors of cytokine signaling 3 (SOCS3) deficiency in neutrophils exacerbates multiple sclerosis (MS) by promoting brain inflammation. This study identifies neutrophil heterogeneity and Saa3 as a potential therapeutic target for autoimmune neuroinflammation.

Keywords:
Brain-targeted Experimental Autoimmune Encephalomyelitis (btEAE)NeutrophilsSAA3 (Serum amyloid A 3)Serum Amyloid A3 (SAA3)Single-cell RNA Sequencing (scRNA-Seq)Suppressors Of Cytokine Signaling 3 (SOCS3)

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Area of Science:

  • Neuroimmunology
  • Autoimmune diseases
  • Central nervous system inflammation

Background:

  • Multiple sclerosis (MS) is an autoimmune demyelinating disease of the central nervous system (CNS).
  • The Janus Kinase (JAK)/Signal Transducers and Activators of Transcription (STAT)/Suppressors Of Cytokine Signaling (SOCS) pathway regulates immune cell activity.
  • SOCS proteins act as negative regulators within this pathway.

Purpose of the Study:

  • To define the specific roles of neutrophils in MS pathogenesis by investigating the function of SOCS3 in these cells.
  • To generate and analyze mice with SOCS3 deletion restricted to neutrophils (Socs3ΔLy6G) in an experimental autoimmune encephalomyelitis (EAE) model of MS.
  • To identify potential therapeutic targets for autoimmune neuroinflammation.

Main Methods:

  • Generation of neutrophil-specific Socs3-deficient mice (Socs3ΔLy6G).
  • Induction of MOG-induced EAE to model MS.
  • Analysis of clinical symptoms, CNS pathology, neutrophil phenotype, and gene expression using Single-cell RNA Sequencing (scRNA-Seq).

Main Results:

  • Socs3ΔLy6G mice exhibited severe cerebellar demyelination and increased infiltration of activated neutrophils and CD4+ T-cells, mirroring severe MS phenotypes.
  • Neutrophils from these mice showed a primed, inflammatory phenotype with elevated reactive oxygen species, neutrophil extracellular traps (NETs), and pro-inflammatory mediators.
  • scRNA-Seq revealed distinct neutrophil clusters (Neu2, Neu4) with upregulated inflammatory genes, including Saa3, which was significantly elevated in the CNS and plasma of affected mice and MS patients.

Conclusions:

  • SOCS3 deficiency in neutrophils unleashes pathogenic activity, contributing to severe autoimmune neuroinflammation in the CNS.
  • Neutrophil heterogeneity exists within the inflamed CNS, with specific transcriptional states associated with inflammation.
  • Saa3/SAA1 emerges as a potential biomarker and therapeutic target for mitigating autoimmune neuroinflammation in MS.