To investigate the pathogenic contributions of AQP4-specific Tfh and Th17 cells in neuromyelitis optica spectrum disorder (NMOSD) using murine models, with a focus on the role of CXCL9 in CNS inflammation.
Key Findings:
Recipient mice developed progressive hind-limb weakness, with Th17-transferred mice showing more severe clinical scores.
Histopathological analyses revealed significant perivascular inflammation, immune infiltration (including T and B lymphocytes), and focal demyelination.
CXCL9 was identified as one of the most upregulated chemokines in the spinal cord, with astrocytic origin confirmed.
Interpretation:
The study establishes that AQP4-specific Tfh and Th17 cells drive key neuropathological features of NMOSD, with CXCL9 playing a significant role in CNS inflammation.
Limitations:
The study primarily utilizes murine models, which may not fully replicate human NMOSD pathology.
The findings are based on a limited sample size of human tissue, which may affect the generalizability of the results.
Conclusion:
AQP4-specific Tfh and Th17 cells contribute to NMOSD pathology, with CXCL9 being a potential contributor to CNS inflammation.
