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Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses
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Basic Science and Pathogenesis.

Nazaret Gamez1, Abdulmunaim M Eid1, Belen Pascual1

  • 1Houston Methodist Research Institute, Houston, TX, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 23, 2025
PubMed
Summary
This summary is machine-generated.

Frontotemporal dementia (FTD) patients show impaired regulatory T cell (Treg) function and increased inflammation, particularly involving the CXCL10/CXCR3 pathway. Targeting this pathway may reduce neuroinflammation and T cell infiltration in the brain.

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Area of Science:

  • Neuroimmunology
  • Neurodegeneration
  • Frontotemporal Dementia (FTD)

Background:

  • Inflammation plays a role in neurodegeneration, but its peripheral immune system's role in FTD is unclear.
  • This study investigates regulatory T cells (Tregs), monocytes, and plasma inflammatory markers in non-fluent variant primary progressive aphasia (nfvPPA), an FTD subtype.

Purpose of the Study:

  • To assess Treg suppressive function in nfvPPA patients.
  • To analyze the inflammatory profile of peripheral monocytes in nfvPPA.
  • To measure plasma inflammatory markers in nfvPPA.

Main Methods:

  • Assessed Treg suppressive function via proliferation assays.
  • Analyzed monocyte gene expression using Nanostring and qRT-PCR.
  • Measured plasma cytokines with Olink® Target 48 panel.
  • Utilized CyTOF for PBMC immunoprofiles and signaling pathway analysis.

Main Results:

  • nfvPPA patients had reduced Treg suppressive function.
  • nfvPPA monocytes showed increased pro-inflammatory gene expression (C1q, NLRP3, PRG3, CXCL10).
  • Elevated plasma CXCL10 and identified CXCL10/CXCR3 pathway activation in nfvPPA.
  • CXCL10 on monocytes and CXCR3 on T cells; CXCL10 promoted T cell inflammation, blocked by AMG487.

Conclusions:

  • nfvPPA is linked to impaired Treg function and systemic CXCL10/CXCR3 pathway activation.
  • This pathway may facilitate T cell homing to the brain.
  • Therapeutic strategies could involve restoring Treg function and targeting CXCL10/CXCR3 to reduce neuroinflammation and T cell infiltration.