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Giant cell arteritis (GCA) is the most frequent vasculitis in people >50 years, and glucocorticoids (GC) remain the cornerstone of the treatment. However, this long-term treatment is responsible for numerous GC-related complications.1 Thus, reliable GC-sparing drugs need to be explored. Seror et al2 have recently reported the inefficacy of adalimumab, a humanised anti-TNF-α therapy, as a GC-sparing drug in the treatment of GCA. These clinical results contrast with previous studies reporting a production of TNF-α by giant cells and macrophages in GCA lesions.3 However, recent advance in the knowledge of GCA pathogenesis have shown that macrophages and giant cells are not involved in the first steps of GCA pathogenesis as they are recruited following CD4 T cells infiltration.4 ,5 We recently demonstrated that CD4CD161+ T lymphocytes largely infiltrate GCA lesions generating Th1 and Th17 cells, and play a major role in GCA pathogenesis.4–,6 Thus, we investigated the …
Collaborators Malika Trad; Marion Ciudad; Alexandrine Gautheron; Famky Seaphanh; Daniela Lakomy.
Contributors Conception, analysis and interpretation of data: MS, SA, NJ, BB. Drafting the article: MS, SA, NJ, BB. Final approval: MS, SA, NJ, BB.
Funding This work was supported by grants from the University Hospital of Dijon, the Direction de la Recherche Clinique and the Conseil Régional de Bourgogne 2010.
Competing interests None.
Ethics approval The study (2009-A00534-53) was approved by the Institutional Review Board and the Ethic Committee of the university hospital of Dijon.
Provenance and peer review Not commissioned; externally peer reviewed.
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