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giant cell arteritis/tyrosine
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Reactive nitrogen intermediates in giant cell arteritis: selective nitration of neocapillaries.
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Arterial wall damage in giant cell arteritis (GCA) is mediated by several different macrophage effector functions, including the production of metalloproteinases and lipid peroxidation. Tissue-invading macrophages also express nitric oxide synthase (NOS)-2, but it is not known whether nitric
PTPN22 R620W minor allele is a genetic risk factor for giant cell arteritis.
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Giant cell arteritis (GCA) is one of the commonest forms of vasculitis in the elderly, and may result in blindness and stroke. The pathogenesis of GCA is not understood, although environmental, infectious and genetic risk factors are implicated. One gene of interest is PTPN22, encoding lymphoid
New insights into the pathogenesis of giant cell arteritis and hopes for the clinic.
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Giant cell arteritis is a complex immune-mediated disease that involves large blood vessels in individuals older than 50 years. Recent studies have confirmed a strong association of this form of vasculitis with the HLA region, particularly with HLA class II genes. However, other non-HLA loci, such
Association between the functional PTPN22 G788A (R263Q) polymorphism and susceptibility to autoimmune diseases: A meta-analysis.
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This study explored whether the functional protein tyrosine phosphatase nonreceptor 22 (PTPN22) G788A (R263Q) polymorphism is associated with susceptibility to autoimmune diseases. A meta-analysis was conducted using 23 comparative studies with a total of 16,719 patients and 17,783 controls. The
Association of PTPN22 1858C/T Polymorphism with Autoimmune Diseases: A Systematic Review and Bayesian Approach.
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The 1858T allele in the protein tyrosine phosphatase non-receptor type 22 (PTPN22) locus shows one of the strongest and most consistent genetic associations with autoimmune diseases. We synthesized all meta-analyses reporting a genetic association of the PTPN22 1858T C/T polymorphism with autoimmune
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