Correlations between histopathological findings and clinical manifestations in biopsy-proven giant cell arteritis

Muratore, Francesco; Boiardi, Luigi; Cavazza, Alberto; Aldigeri, Raffaella; Pipitone, Nicolò; Restuccia, Giovanna; Bellafiore, Salvatore; Cimino, Luca; Salvarani, Carlo

doi:10.1016/j.jaut.2016.03.005

Cited by 34 publications

(32 citation statements)

References 31 publications

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“…With the exception of 3 studies , a vast number of studies have shown that GCA patients with a strong systemic inflammatory response have a lower risk of cranial ischemic symptoms compared with patients with a weak systemic inflammatory response (Table ) . For instance, pretreatment ESRs and CRP levels are inversely correlated with the risk of visual symptoms in GCA (). The presence of fever is also associated with a lower risk of cranial ischemia in GCA patients .…”

Section: Evidence For Distinct Gca Subsets Based On Clinical Featuresmentioning

confidence: 99%

“…Macrophages around the internal elastic membrane are activated by Th1 cells and CD8+ T cells and develop into multinucleated giant cells under the influence of IFNγ . The presence of giant cells was associated with an increased risk of cranial ischemia in 2 studies , and also tended to correlate with more cranial ischemic symptoms in a third study . Macrophages and giant cells near the internal elastic membrane may secrete platelet‐derived growth factor (PDGF) and VEGF, which activate VSMCs .…”

Section: Evidence For Distinct Gca Subsets Based On Immunologic Featuresmentioning

confidence: 99%

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Review: What Is the Current Evidence for Disease Subsets in Giant Cell Arteritis?

Geest

Sandovici

Sleen

et al. 2018

Arthritis & Rheumatology

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Giant cell arteritis (GCA) is an autoimmune vasculitis affecting large and medium‐sized arteries. Ample evidence indicates that GCA is a heterogeneous disease in terms of symptoms, immune pathology, and response to treatment. In the current review, we discuss the evidence for disease subsets in GCA. We describe clinical and immunologic characteristics that may impact the risk of cranial ischemic symptoms, relapse rates, and long‐term glucocorticoid requirements in patients with GCA. In addition, we discuss both proven and putative immunologic targets for therapy in patients with GCA who have an unfavorable prognosis. Finally, we provide recommendations for further research on disease subsets in GCA.

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Section: Evidence For Distinct Gca Subsets Based On Clinical Featuresmentioning

confidence: 99%

Section: Evidence For Distinct Gca Subsets Based On Immunologic Featuresmentioning

confidence: 99%

Review: What Is the Current Evidence for Disease Subsets in Giant Cell Arteritis?

Geest

Sandovici

Sleen

et al. 2018

Arthritis & Rheumatology

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“…This holds true specifically for blindness‐inducing ischemic optic neuropathy. Cellular origins and processes giving rise to the growing intima are not entirely clear, but proceed at rapid pace in GCA . Arteries treated with the checkpoint inhibitor had markedly increased numbers of microvessels and the thickness of the intimal layer doubled .…”

Section: Insufficiently Suppressed T Cells In Gcamentioning

confidence: 99%

The immunoinhibitory PD-1/PD-L1 pathway in inflammatory blood vessel disease

Weyand

Berry

Goronzy

2017

Journal of Leukocyte Biology

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Because of their vital function, the wall structures of medium and large arteries are immunoprivileged and protected from inflammatory attack. That vascular immunoprivilege is broken in atherosclerosis and in vasculitis, when wall-invading T cells and macrophages (Mϕ) promote tissue injury and maladaptive repair. Historically, tissue-residing T cells were studied for their antigen specificity, but recent progress has refocused attention to antigen-nonspecific regulation, which determines tissue access, persistence, and functional differentiation of T cells. The coinhibitory receptor PD-1, expressed on T cells, delivers negative signals when engaged by its ligand PD-L1, expressed on dendritic cells, Mϕ, and endothelial cells to attenuate T cell activation, effector functions, and survival. Through mitigating signals, the PD-1 immune checkpoint maintains tissue tolerance. In line with this concept, dendritic cells and Mϕs from patients with the vasculitic syndrome giant cell arteritis (GCA) are PD-L1 ; including vessel-wall-embedded DCs that guard the vascular immunoprivilege. GCA infiltrates in the arterial walls are filled with PD-1 T cells that secrete IFN-γ, IL-17, and IL-21; drive inflammation-associated angiogenesis; and facilitate intimal hyperplasia. Conversely, chronic tissue inflammation in the atherosclerotic plaque is associated with an overreactive PD-1 checkpoint. Plaque-residing Mϕs are PD-L1 , a defect induced by their addiction to glucose and glycolytic breakdown. PD-L1 Mϕs render patients with coronary artery disease immunocompromised and suppress antiviral immunity, including protective anti-varicella zoster virus T cells. Thus, immunoinhibitory signals affect several domains of vascular inflammation; failing PD-L1 in vasculitis enables unopposed immunostimulation and opens the flood gates for polyfunctional inflammatory T cells, and excess PD-L1 in the atherosclerotic plaque disables tissue-protective T cell immunity.

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“…By multivariate logistic regression, the absence of high levels of ESR (> 96 mm/h) at the time of disease diagnosis was the best predictor for development of permanent visual loss 6 . A recent study of this group also indicates that, besides calcifications at temporal artery biopsy, lower CRP values are also predictors for development of permanent visual loss 11 . Cid, et al also found that the mean ESR was significantly reduced in their patients with irreversible cranial ischemic complications compared with the rest of the patients with biopsy-proven GCA 12 .…”

mentioning

confidence: 87%