REVIEW article
Front. Immunol.
Sec. Autoimmune and Autoinflammatory Disorders: Autoinflammatory Disorders
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1608402
This article is part of the Research TopicCommunity Series in Prognostic and Predictive Factors in Autoimmune Connective Tissue Disorders Volume IIView all 5 articles
The Role of Calprotectin in Giant Cell Arteritis -From Pathophysiology to Possible Clinical Applications
Provisionally accepted
- National Institute of Geriatrics, Rheumatology and Rehabilitation, Warsaw, Poland
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Giant cell arteritis (GCA) is an immune-mediated vasculitis predominantly affecting individuals aged 50 years and older, with clinical manifestations often overlapping with polymyalgia rheumatica (PMR). Despite advances in imaging and the advent of novel steroid-sparing agents, such as tocilizumab, challenges persist in accurately diagnosing and monitoring disease activity. Traditional inflammatory markers like C-reactive protein and erythrocyte sedimentation rate are frequently limited by their inability to fully capture disease dynamics, especially in patients receiving IL-6 inhibitors. In this context, calprotectin (CLP), a heterodimeric complex derived from S100A8/S100A9 proteins, has emerged as a promising biomarker due to its integral role in mediating inflammatory responses and its relative independence from IL-6 pathways. This review synthesizes current evidence on the biological functions of CLP in GCA pathogenesis, its potential utility in distinguishing between different clinical forms of the GCA-PMR spectrum, and its role in assessing disease activity and guiding therapeutic decisions. Furthermore, emerging CLP-targeted therapies in other inflammatory conditions may offer novel treatment avenues for GCA. Future research should focus on validating CLP as a predictive marker for relapse and refining its integration into clinical monitoring protocols to enhance patient outcomes.
Keywords: Giant Cell Arteritis, calprotectin, biomarker, disease activity, diagnosis
Received: 08 Apr 2025; Accepted: 28 Jul 2025.
Copyright: © 2025 Kudraszew, Roszkowski, Ciechomska and Wroński. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Jakub Wroński, National Institute of Geriatrics, Rheumatology and Rehabilitation, Warsaw, Poland
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