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Related Concept Videos

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Specific Follicular Helper T Cell Signature in Takayasu Arteritis.

A C Desbois1, P Régnier1, V Quiniou2

  • 1Sorbonne Université, Centre National de Références Maladies Autoimmunes et Systémiques Rares et Maladies Autoinflammatoires Rares, INSERM UMR 959, Groupe Hôpital Pitié-Salpêtrière, AP-HP, Paris, France.

Arthritis & Rheumatology (Hoboken, N.J.)
|February 4, 2021
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Summary

A specific follicular helper T (Tfh) cell signature is present in Takayasu arteritis (TAK) patients, driving B cell activation and IgG secretion, potentially causing vascular inflammation.

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Area of Science:

  • Immunology
  • Vascular Biology
  • Genomics

Background:

  • Takayasu arteritis (TAK) and giant cell arteritis (GCA) are large vessel vasculitides with distinct clinical and etiological profiles.
  • Understanding the cellular and molecular mechanisms underlying TAK pathogenesis is crucial for developing targeted therapies.

Purpose of the Study:

  • To compare the transcriptome and phenotype profiles of CD4+ T cells and CD19+ B cells in patients with TAK, GCA, and healthy donors.
  • To identify specific immune cell signatures associated with TAK pathogenesis.

Main Methods:

  • Gene expression analysis, flow cytometry, T cell receptor sequencing, and functional cell assessments were performed.
  • Samples were obtained from peripheral blood and arterial lesions of TAK patients, GCA patients, and healthy donors.

Main Results:

  • A follicular helper T (Tfh) cell signature, including CXCR5, CCR6, and CCL20 genes, was transcriptionally upregulated in CD4+ T cells of TAK patients.
  • An increase in CD4+CXCR5+CCR6+CXCR3- Tfh17 cells in TAK patients correlated with enhanced CD19+ B cell activation.
  • Tertiary lymphoid structures with CD4+, CXCR5+, PD-1+, and CD20+ cells were more prevalent in arterial lesions of TAK patients.

Conclusions:

  • A distinct Tfh cell signature exists in circulating and aorta-infiltrating CD4+ T cells of TAK patients.
  • Tfh cell and B cell cooperation may play a critical role in the vascular inflammation observed in TAK.