HLA antigens and complement types in patients with intracranial saccular aneurysms

Østergaard, John R.; Bruun‐Petersen, G.; Lamm, L. U.

doi:10.1111/j.1399-0039.1986.tb00478.x

Cited by 30 publications

(2 citation statements)

References 22 publications

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“…The genetic associations between HLA molecules and the pathogenesis of IAs have been widely debated in the last century ( Lye and Dyer, 1989 ; Lye et al, 1989 ), but little research has been conducted recently. Ostergaard et al (1986) found that HLA-DR2 antigen frequency is significantly increased (66.7% vs. 29.7%, p < 0.01) in IAs compared to healthy controls. However, a later study conducted by Schievink et al (1988) revealed no significant difference in the HLA-DR2 frequency between IAs and controls, which was further supported by the findings of Lye and Dyer (1989) .…”

Section: Discussionmentioning

confidence: 84%

Novel insight into m6A regulator-mediated methylation modification patterns and immune characteristics in intracranial aneurysm

Zhang

Weng

et al. 2022

Front. Aging Neurosci.

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BackgroundGrowing evidence demonstrated that m6A modification in cardiovascular diseases. However, how it is involved in the intracranial aneurysm (IA) is still unclear. This study aimed to identify the role of m6A modification in IA.MethodsThree datasets downloaded from the Gene Expression Omnibus (GEO) database were used, including GSE122897, GSE15629, and GSE3679. The landscapes of 24 m6A regulators were depicted using the STRING database, Pearson’s correlation analysis, and Wilcoxon test. The targets of differentially expressed m6A (DEm6A) were predicted in the m6A2Target database and the modification m6A sites of hub targets were identified in SRAMP online tool. A diagnostic model based on DEm6A was constructed and verified in training and test databases. A consensus clustering algorithm was performed to classify IA patients into distinct m6A-related clusters. Functional analyses including gene ontology, Kyoto Encyclopedia of Genes and Genomes (KEGG), gene set variation analysis, and gene set enrichment analysis analyses were conducted to elucidate the underlying mechanisms. ssGSEA algorithm was performed to uncover the immune characteristics. A PCA method was adopted to quantify the m6A score.ResultsNine DEm6A (IGF2BP1, IGF2BP3, YTHDF2, ZNF217, RBM15, YTHDF3, YTHDC1, FTO, and LRPPRC) significantly differed between IA and controls. Biological annotations showed that immune-related pathways (such as complement activation, inflammatory response, and interleukin signaling) and apoptosis were more enriched in IAs than in controls. Immune analyses indicate that the abundance of immune cells, immune responses, and HLA gene expression were elevated in IA samples than in controls. PCA results showed that IA has a lower m6A score than controls. An immune/apoptosis-related network modified by DEm6A was constructed. The m6A sites of six hub targets (CDK1, ASPM, AURKB, BUB1B, MKI67, and TPX2) were predicted with very high confidence. A diagnostic model with four genes (LRPPRC, YTHDF3, IGF2BP1, and ZNF217) was constructed and verified. Two m6A modification subtypes were identified with unsupervised cluster analysis. Immune infiltration analysis revealed that cluster 1 had higher immune activation than cluster 2. Further study showed that cluster 1 had a larger proportion of ruptured IAs.ConclusionThe m6A modification may shape the IAs microenvironment and participates in the formation and rupture of IAs by regulating immune infiltration.

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Section: Discussionmentioning

confidence: 84%

Novel insight into m6A regulator-mediated methylation modification patterns and immune characteristics in intracranial aneurysm

Zhang

Weng

et al. 2022

Front. Aging Neurosci.

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“…A significantly increased frequency of HLA antigen A28, a significantly decreased frequency of both HLA antigen B40 and complement factor C4B2 were found in the serum of IA patients when compared with controls (174). In other association studies, HLA DR2, and DR7 alleles were found to be associated with IA (175, 176).…”

Section: Association Studies Try To Confirm the Candidate Loci Of Iamentioning

confidence: 78%

Molecular Genetics of Human Intracranial Aneurysms

Zhang

Claterbuck

2008

International Journal of Stroke

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Intracranial aneurysms (IAs) are the dilatations of blood vessels in the brain and pose potential risk of rupture leading to subarachnoid hemorrhage. Although the genetic basis of IAs is poorly understood, it is well-known that genetic factors play an important part in the pathogenesis of IAs. Therefore, the identifying susceptible genetic variants might lead to the understanding of the mechanism of formation and rupture of IAs and might also lead to the development of a pharmacological therapy. To elucidate the molecular pathogenesis of diseases has become a crucial step in the development of new treatment strategies. Although extensive genetic research and its potential implications for future prevention of this often fatal condition are urgently needed, efforts to elucidate the susceptibility loci of IAs are hindered by the issues bewildering the most common and complex genetic disorders, such as low penetrance, late onset, and uncertain modes of inheritance. These efforts are further complicated by the fact that many IA lesions remain asymptomatic or go undiagnosed. In this review, we present and discuss the current status of genetic studies of IAs and we recommend comprehensive genome-wide association studies to identify genetic loci that underlie this complex disease.

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Impaired in vitro proliferative response of suppressor lymphocytes in patients with subarachnoid haemorrhage from ruptured intracranial aneurysm

Grieb

Pastuszko

et al. 1993

Acta neurochir

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Proliferative response to mitogens concanavalin A, phytohemagglutinin and pokeweed mitogen, and other chosen indicators of the activity of the immune system were assayed in peripheral blood mononuclear cells isolated from blood of patients with subarachnoid haemorrhage from ruptured aneurysm. Healthy blood donors served as control group. The SAH group displayed impaired response to concanavalin A, which is a mitogen specific for suppressor cells. It is suggested that the impaired activity of suppressor cells pre-existed in patients with subarachnoid haemorrhage, and after intracranial bleeding it might have contributed to the development of late neurological deficits.

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HLA antigens and complement types in patients with intracranial saccular aneurysms

Cited by 30 publications

References 22 publications

Novel insight into m6A regulator-mediated methylation modification patterns and immune characteristics in intracranial aneurysm

Novel insight into m6A regulator-mediated methylation modification patterns and immune characteristics in intracranial aneurysm

Molecular Genetics of Human Intracranial Aneurysms

Impaired in vitro proliferative response of suppressor lymphocytes in patients with subarachnoid haemorrhage from ruptured intracranial aneurysm

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