Gut Microbiome and Bile Acid Metabolism Induced the Activation of CXCR5+ CD4+ T Follicular Helper Cells to Participate in Neuromyelitis Optica Spectrum Disorder Recurrence
CXCL13
CXCR5
Neuromyelitis Optica
DOI:
10.3389/fimmu.2022.827865
Publication Date:
2022-01-20T06:35:22Z
AUTHORS (10)
ABSTRACT
From the perspective of role T follicular helper (Tfh) cells in destruction tolerance disease progression, more attention has been paid to their autoimmunity. To address Tfh neuromyelitis optica spectrum disorder (NMOSD) recurrence, serum C-X-C motif ligand 13 (CXCL13) levels reflect effects on B-cell-mediated humoral immunity. We evaluated immunobiology CXCR5+CD4+ 46 patients with NMOSD, including 37 NMOSD an annual recurrence rate (ARR) of<1 and 9 ARR ≥1. Herein, we reported several key observations. First, there was a lower frequency circulating than those ≥1 (P< 0.05). Second, CXCL13 were downregulated individuals ARR<1 0.05), processing ability promote maturation chemotaxis. Third, level primary bile acid, glycoursodeoxycholic acid (GUDCA), higher ≥1, which positively correlated CXCL13. Lastly, precursor decreased spleen keyhole limpet haemocyanin-stimulated animals following GUDCA intervention. These findings significantly broaden our understanding NMOSD. Our data also reveal potential mechanism intestinal microbiota metabolites involved recurrence.
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