Relationship between interleukin 6 promoter polymorphism at position -174, IL-6 serum levels, and the risk of relapse/recurrence in polymyalgia rheumatica.
To assess the potential protective role of proinflammatory cytokines in the development of ischemic events in GCA, we measured tissue expression (66 individuals) and/or circulating levels (80 individuals) of interleukin (IL)-1beta, tumor necrosis factor-alpha (TNF-alpha), and IL-6 in patients with biopsy-proven GCA.
Diagnostic performance of <sup>18</sup>F-FDG PET-CT for large vessel involvement assessment in patients with suspected giant cell arteritis and negative temporal artery biopsy.
Sequence comparison among the allelic products identified in the GCA cohort demonstrated heterogeneity for the sequence polymorphism of the third hypervariable region (HVR), but homology for the polymorphic residues within the HVR2 of the HLA-DRB1 gene.
GCA seems to be associated with HLA DRB1*04 (regardless of the subtype) and this association appears to be accompanied by corticosteroid resistance, suggesting that genomic typing may be useful to identify patients eligible for early alternative treatment to corticosteroid drugs.
Cell-mediated immunity to VZV was determined by performing interferon-γ (IFNγ) enzyme-linked immunospot and intracellular cytokine flow cytometry measurements in 11 GCA and 15 PMR patients and in 26 age/sex-matched HCs.
Expert commentary: Two randomized controlled trials recently showed the efficacy of the IL-6 receptors inhibitor monoclonal antibody TCZ for the induction and maintenance of remission in patients with new-onset and relapsing GCA.
GCA incidence (n = 17 countries) was associated with population HLA-DRB1*04 allele frequency (P = 0.008; adjusted R(2) = 0.51 on univariable analysis, adjusted R(2) = 0.62 after also including latitude); latitude also made an independent contribution.
A multivariate model including class II amino acids of HLA-DRβ1 and HLA-DQα1 and one class I amino acid of HLA-B explained most of the HLA association with GCA, consistent with previously reported associations of classical HLA alleles like HLA-DRB1(∗)04.