Use of high-plex data provides novel insights into the temporal artery processes of giant cell arteritis

Parreau, Simon; Molina, Elsa; Dumonteil, Stéphanie; Goulabchand, Radjiv; Naves, Thomas; Bois, Melanie C.; Akil, Hussein; Terro, Faraj; Fauchais, Anne-Laure; Liozon, Eric; Jauberteau, Marie-Odile; Weyand, Cornelia M.; Ly, Kim-Heang

doi:10.3389/fimmu.2023.1237986

Cited by 3 publications

(3 citation statements)

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“…In a recent study using spatial transcriptomics, CD74 (HLA class-II histocompatibility antigen) was identified as the most differentially expressed gene across all arterial compartments between GCA-arteries (n=9) and controls (n=7). 114 Additionally, immunofluorescence staining showed CD74 to colocalise with the fibroblast marker CD90 in the media-intima border. 114 Greigert et al also demonstrated that myofibroblasts significantly expressed HLA-DR, compared with controls.…”

Section: Reviewmentioning

confidence: 98%

“…114 Additionally, immunofluorescence staining showed CD74 to colocalise with the fibroblast marker CD90 in the media-intima border. 114 Greigert et al also demonstrated that myofibroblasts significantly expressed HLA-DR, compared with controls. 23 Stromal cells can express MHC class II molecules in response to inflammatory stimuli 115 116 ; however, whether they have the capacity to induce T-cell proliferation analogous to conventional antigen-presenting cells remains unclear.…”

Section: Reviewmentioning

confidence: 98%

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Vascular disease persistence in giant cell arteritis: are stromal cells neglected?

Karabayas,

Ibrahim,

Roelofs

et al. 2024

Ann Rheum Dis

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Giant cell arteritis (GCA), the most common systemic vasculitis, is characterised by aberrant interactions between infiltrating and resident cells of the vessel wall. Ageing and breach of tolerance are prerequisites for GCA development, resulting in dendritic and T-cell dysfunction. Inflammatory cytokines polarise T-cells, activate resident macrophages and synergistically enhance vascular inflammation, providing a loop of autoreactivity. These events originate in the adventitia, commonly regarded as the biological epicentre of the vessel wall, with additional recruitment of cells that infiltrate and migrate towards the intima. Thus, GCA-vessels exhibit infiltrates across the vascular layers, with various cytokines and growth factors amplifying the pathogenic process. These events activate ineffective repair mechanisms, where dysfunctional vascular smooth muscle cells and fibroblasts phenotypically shift along their lineage and colonise the intima. While high-dose glucocorticoids broadly suppress these inflammatory events, they cause well known deleterious effects. Despite the emerging targeted therapeutics, disease relapse remains common, affecting >50% of patients. This may reflect a discrepancy between systemic and local mediators of inflammation. Indeed, temporal arteries and aortas of GCA-patients can show immune-mediated abnormalities, despite the treatment induced clinical remission. The mechanisms of persistence of vascular disease in GCA remain elusive. Studies in other chronic inflammatory diseases point to the fibroblasts (and their lineage cells including myofibroblasts) as possible orchestrators or even effectors of disease chronicity through interactions with immune cells. Here, we critically review the contribution of immune and stromal cells to GCA pathogenesis and analyse the molecular mechanisms by which these would underpin the persistence of vascular disease.

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Section: Reviewmentioning

confidence: 98%

Section: Reviewmentioning

confidence: 98%

Vascular disease persistence in giant cell arteritis: are stromal cells neglected?

Karabayas,

Ibrahim,

Roelofs

et al. 2024

Ann Rheum Dis

View full text Add to dashboard Cite

show abstract

“…Over 12000 genes were found to be upregulated in the arteries, with differential expression according to different arterial layers. Interestingly, the immune-related functions and vascular remodeling were limited to the intima and media (26). A genetic approach was also used to estimate the proportion of misdiagnosis in patients with a clinically confirmed diagnosis of GCA, not supported by TAB or imaging.…”

Section: Biomarkers and Implications In Thepathogenesismentioning

confidence: 99%