6533b856fe1ef96bd12b3264
RESEARCH PRODUCT
Is TNF-α really involved in giant cell arteritis pathogenesis?
Bernard BonnotteBernard BonnotteMaxime SamsonMaxime SamsonSylvain AudiaSylvain AudiaNona JanikashviliNona Janikashvilisubject
CD4-Positive T-LymphocytesMaleImmunologyGiant Cell ArteritisGeneral Biochemistry Genetics and Molecular BiologyPathogenesisRheumatologyimmune system diseasesAdalimumabImmunology and AllergyMedicineHumanscardiovascular diseasesskin and connective tissue diseasesAgedAged 80 and overbusiness.industryTumor Necrosis Factor-alphaMiddle Agedmedicine.diseaseGiant cell arteritisGiant cellImmunologycardiovascular systemTumor necrosis factor alphaFemalebusinessVasculitismedicine.drugdescription
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 al 2 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 …
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2013-08-29 | Annals of the rheumatic diseases |