Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

HLA-DR locus antigens were determined in 69 patients with giant cell arteritis, polymyalgia rheumatica, or both. The frequencies of HLA-DR4 and HLA-DRW6 in these patients were increased above normals. But the differences were not significant in the total group nor when the patients were separated according to the presence or absence of polymyalgia rheumatica.
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PMID:HLA-DR locus antigens in polymyalgia rheumatica and giant cell arteritis. 694 60

Molecular techniques have provided new tools to define genetic systems involved in disease susceptibility and to dissect molecular events driving inflammatory reactions. Inflammatory infiltrates in the wall of large and medium-sized arteries, sometimes associated with giant cell formation, are pathognomic for Takayasu's arteritis (TA) and giant cell (cranial) arteritis. Molecular techniques have been used successfully to define genetic host factors involved in disease susceptibility and to dissect the nature of inflammatory cells and mediators in the pathologic lesions. Careful analysis of incidence data for TA suggests that TA is a worldwide disease. Genetic comparison of western and eastern TA, however, raises the possibility of disease heterogeneity. Emerging data indicate that HLA-DRB1 genes represent important risk factors in giant cell arteritis. Whether disease association is related to the role of HLA-DR molecules in presenting a disease-inducing antigen remains to be seen. Analysis of the molecular diversity of tissue-infiltrating T cells indicates that a small proportion of CD4+ T cells proliferate in situ, potentially as a result of antigen recognition. Tissue cytokine profiles reveal functional selection of T cells and are compatible with the model that Th1 cells recognize antigen on the surface of activated macrophages. The presence of T cell-derived cytokines in temporal artery tissue of patients with polymyalgia rheumatica who are lacking microscopic inflammation indicates subclinical vasculitis.
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PMID:Molecular approaches toward pathologic mechanisms in giant cell arteritis and Takayasu's arteritis. 771 19

Emerging data support the model that giant cell arteritis (GCA) is an antigen-driven disease. Select helper T cells are recruited to the vascular lesions where they produce a defined pattern of cytokines. At least two functionally distinct populations of macrophages are involved and macrophage activation extends into the compartment of circulating phagocytes. Searches for the antigen may be facilitated through structural analysis of specially activated T lymphocytes in the lesions. In addition to the proposed disease-inducing agent, genetic risk factors are important. One of the genetic elements has been mapped to the HLA-DR region and seems to encode parts of a pocket in the HLA-DR molecule, accommodating side chains of the interacting antigenic peptide. On the molecular level, some but not all pathomechanisms are shared by polymyalgia rheumatica and GCA, indicating that both syndromes form a spectrum of disease.
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PMID:Giant cell arteritis as an antigen-driven disease. 859 35

Giant cell arteritis is the most frequent of all vasculitides. Estimates of its incidence lies between 10 and 20 cases/100,000/year, and estimates of its prevalence in the population over 50 between 100 and 200/100,000/year. Giant cell arteritis affects primarily patients over 50, and the increased prevalence among women, partially reflects the sex distribution in this age group. The cause of the disease remains unknown, but a genetic predisposition (HLA-DR 4 group), has been clearly shown. Seasonal, and annual peaks of incidence have been shown in some studies, suggesting an infectious or environmental etiologic factor.
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PMID:[Nosology and epidemiology of Horton's disease and polymyalgia rheumatica]. 1021 92

Emerging evidence implicating the participation of dendritic cells (DCs) and T cells in various vascular inflammatory diseases such as giant cell arteritis, Takayasu's arteritis, and atherosclerosis led us to hypothesize that they might also participate in the pathogenesis of coronary arteritis in Kawasaki disease (KD). Coronary artery specimens from 4 patients with KD and 6 control patients were obtained. Immunohistochemical and computer-assisted histomorphometric analyses were performed to detect all myeloid DCs (S-100(+), fascin(+)), all plasmacytoid DCs (CD123(+)) as well as specific DC subsets (mature myeloid DCs [CD83(+)], myeloid [BDCA-1(+)] and plasmacytoid DC precursors [BDCA-2(+)]), T cells (CD3(+)), and all antigen-presenting cells (HLA-DR(+)). Co-localization of DCs with T cells was assessed using double immunostaining. Significantly more myeloid DCs at a precursor, immature or mature stage were found in coronary lesions of KD patients than in controls. Myeloid DC precursors were distributed equally in the intima and adventitia. Mature myeloid DCs were particularly abundant in the adventitia. There was a significant correlation between mature DCs and HLA-DR expression. Double immunostaining demonstrated frequent contacts between myeloid DCs and T cells in the outer media and adventitia. Plasmacytoid DC precursors were rarely found in the adventitia. In conclusion, coronary artery lesions of KD patients contain increased numbers of mature myeloid DCs with high HLA-DR expression and frequent T cell contacts detected immunohistochemically. This suggests that mature arterial myeloid DCs might be activating T cells in situ and may be a significant factor in the pathogenesis of coronary arteritis in KD.
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PMID:Activated myeloid dendritic cells accumulate and co-localize with CD3+ T cells in coronary artery lesions in patients with Kawasaki disease. 1733 4


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