Scholarlink

<p>Autoinflammation of unknown origin remains amongst the most enigmatic of systemic autoinflammatory disorders (SAID), with systemic autoinflammatory symptoms in the absence of a molecular or clinical diagnosis with a recognized SAID. Here, we aim to understand the immunological process behind patients with autoinflammation of unknown origin. We collect samples from 36 patients manifesting recent disease activity across 30 European medical centers, and employ deep immunophenotyping and plasma proteomics to compare to 58 healthy controls and an additional demographically similar cohort comprising 92 SAID patients. Machine-learning approaches identify key immunological changes, including the upregulation of CD38 and HLA across T cell subsets and the upregulation of acute-phase plasma proteins in autoinflammation of unknown origin patients. The immunological traits of these previously poorly characterised patients partially phenocopy Still’s disease presentation. Thus, this study identifies potential biomarkers and disease mediators in autoinflammation of unknown origin.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Adult patients with autoinflammation of unknown origin partially phenocopy the immune presentation of Still’s disease

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月1日

查看全文
  • Rafael Veiga,
  • Leana De Vuyst,
  • Christophe Poulet,
  • Julika Neumann,
  • Leoni Bücken,
  • Teresa Prezzemolo,
  • Mathijs Willemsen,
  • Steven Vanderschueren,
  • Patrick Matthys,
  • Emna Chabaane,
  • Maximilien Fléron,
  • Gaël Cobraiville,
  • Dominique Baiwir,
  • Gabriel Mazzucchelli,
  • Bruno Fautrel,
  • Carine Wouters,
  • Dominique De Seny,
  • Stephanie Humblet-Baron,
  • Adrian Liston

摘要

Autoinflammation of unknown origin remains amongst the most enigmatic of systemic autoinflammatory disorders (SAID), with systemic autoinflammatory symptoms in the absence of a molecular or clinical diagnosis with a recognized SAID. Here, we aim to understand the immunological process behind patients with autoinflammation of unknown origin. We collect samples from 36 patients manifesting recent disease activity across 30 European medical centers, and employ deep immunophenotyping and plasma proteomics to compare to 58 healthy controls and an additional demographically similar cohort comprising 92 SAID patients. Machine-learning approaches identify key immunological changes, including the upregulation of CD38 and HLA across T cell subsets and the upregulation of acute-phase plasma proteins in autoinflammation of unknown origin patients. The immunological traits of these previously poorly characterised patients partially phenocopy Still’s disease presentation. Thus, this study identifies potential biomarkers and disease mediators in autoinflammation of unknown origin.