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Is TNF-α really involved in giant cell arteritis pathogenesis?
  1. Maxime Samson1,2,3,
  2. Sylvain Audia1,2,3,
  3. Nona Janikashvili1,2,3,
  4. Bernard Bonnotte1,2,3
  1. 1Service de Médecine Interne et Immunologie Clinique, CHU de Dijon, 2 Bd Mal de Lattre de Tassigny, Dijon, France
  2. 2INSERM, UMR1098, Besançon, Cedex, France
  3. 3Université de Bourgogne, Faculté de Médecine, Dijon, France
  1. Correspondence to Professor Bernard Bonnotte, Service de Médecine Interne et Immunologie Clinique, CHU Dijon le Bocage, 2 Bd Mal de Lattre de Tassigny, Dijon 21000, France; Bernard.bonnotte{at}chu-dijon.fr

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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 …

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