HLA DR4 and giant cell arteritis

Bignon, Jean-Denis; Barrier, J; Soulillou, Jean‐Paul; Martin, Philippe; Grolleau, J.Y.

doi:10.1111/j.1399-0039.1984.tb00399.x

Cited by 27 publications

(1 citation statement)

References 9 publications

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“…There is a strong association between GCA and the human leukocyte antigen (HLA) region, which highlights the essential role of adaptive immunity in the pathogenesis of this vasculitis. Alleles of HLA-DRB1*04 , particularly the HLA-DRB1*0401 , DRB1*0404 or DRB1*0408 haplotypes, have been shown to be associated with the occurrence of GCA in independent cohorts [ 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 ] and are expressed by 60% of patients affected by polymyalgia rheumatica (PMR) or GCA [ 18 , 24 , 28 ]. These haplotypes are thought to be responsible for the selection of peptides involved in the GCA pathogenesis that are then presented to CD4 + T cells.…”

Section: Implications Of Genetic Background Epigenetics and Agingmentioning

confidence: 99%

New Insights into the Pathogenesis of Giant Cell Arteritis: Mechanisms Involved in Maintaining Vascular Inflammation

Greigert

Genet

Bonnotte

et al. 2022

JCM

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The giant cell arteritis (GCA) pathophysiology is complex and multifactorial, involving a predisposing genetic background, the role of immune aging and the activation of vascular dendritic cells by an unknown trigger. Once activated, dendritic cells recruit CD4 T cells and induce their activation, proliferation and polarization into Th1 and Th17, which produce interferon-gamma (IFN-γ) and interleukin-17 (IL-17), respectively. IFN-γ triggers the production of chemokines by vascular smooth muscle cells, which leads to the recruitment of additional CD4 and CD8 T cells and also monocytes that differentiate into macrophages. Recent data have shown that IL-17, IFN-γ and GM-CSF induce the differentiation of macrophage subpopulations, which play a role in the destruction of the arterial wall, in neoangiogenesis or intimal hyperplasia. Under the influence of different mediators, mainly endothelin-1 and PDGF, vascular smooth muscle cells migrate to the intima, proliferate and change their phenotype to become myofibroblasts that further proliferate and produce extracellular matrix proteins, increasing the vascular stenosis. In addition, several defects in the immune regulatory mechanisms probably contribute to chronic vascular inflammation in GCA: a defect in the PD-1/PD-L1 pathway, a quantitative and qualitative Treg deficiency, the implication of resident cells, the role of GM-CSF and IL-6, the implication of the NOTCH pathway and the role of mucosal‑associated invariant T cells and tissue‑resident memory T cells.

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Section: Implications Of Genetic Background Epigenetics and Agingmentioning

confidence: 99%

New Insights into the Pathogenesis of Giant Cell Arteritis: Mechanisms Involved in Maintaining Vascular Inflammation

Greigert

Genet

Bonnotte

et al. 2022

JCM

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Hla‐dr4 in giant cell arteritis: association with polymyalgia rheumatica syndrome

Richardson

Gladman

Fam

et al. 1987

Arthritis & Rheumatism

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Forty-three patients with well-documented giant cell arteritis (GCA) were studied clinically and with HLA typing. All patients were over age 40. Twenty-two of the patients had coexistent polymyalgia rheumatica (PMR). No association with class I HLA antigens was detected. When compared with HLA findings in 243 healthy controls, HLA-DR4 was increased in patients with GCA and PMR, but not in patients with GCA alone. Pooled analysis of data from 4 published papers confirmed the association of DR4 with GCA and PMR (P <

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Polymyalgia rheumatica: a syndrome associated with hla–dr4 antigen

Ercilla

Vilaseca

et al. 1988

Arthritis & Rheumatism

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HLA class II antigens were determined in 65 patients with biopsy‐proven giant cell arteritis (GCA). An increase in DR4 antigen frequency was found in the patients (40%) compared with that in 200 healthy controls (20%) (Pcorr < 0.05). DR4 was significantly more frequent in GCA patients with polymyalgia rheumatica (PMR) than in those without PMR (58.8% versus 19.3%) (P < 0.005). HLA–DR4 frequency in GCA patients without PMR was similar to that in the control population (20%). Patients with severe, disabling PMR had DR4 more frequently (90%) than did those with moderate symptoms who required medical care because of cranial arteritis manifestations (41.6%) (P < 0.05). We conclude that, in GCA patients, association with DR4 is mainly related to the manifestation of the disease as PMR. We discuss clinical and immunogenetic similarities between PMR and other DR4‐associated rheumatic disorders. Common immunopathogenic mechanisms leading to clinical overlap among them are suggested.

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HLA DR4 and giant cell arteritis

Cited by 27 publications

References 9 publications

New Insights into the Pathogenesis of Giant Cell Arteritis: Mechanisms Involved in Maintaining Vascular Inflammation

New Insights into the Pathogenesis of Giant Cell Arteritis: Mechanisms Involved in Maintaining Vascular Inflammation

Hla‐dr4 in giant cell arteritis: association with polymyalgia rheumatica syndrome

Polymyalgia rheumatica: a syndrome associated with hla–dr4 antigen

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