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001-es BibID:BIBFORM007058
Első szerző:Faragó Bernadett
Cím:Protein tyrosine phosphatase gene C1858T allele confers risk for rheumatoid arthritis in Hungarian subjects / Farago, B., Talian, G. C., Komlosi, K., Nagy, G., Berki, T., Gyetvai, A., Szekanecz, Z., Nyarady, Z., Kiss, C. G., Nemeth, P., Czirjak, L., Melegh, B.
Dátum:2009
ISSN:1437-160X
Megjegyzések:The C1858T allele of the PTPN22 gene has been reported to confer risk for RA; but in some reports, the effect was restricted to RF- and/or anti-CCP-seropositive patients. Hungarian RA patients and matched controls were genotyped. The 1858T allele showed an increased prevalence in RA patients compared to controls. The 1858T allele represents a risk factor in the whole RA population (P = 0.001); an association was found both in RF-seropositive (P = 0.001) and anti-CCP-seropositive patients (P = 0.001), and in subjects with the combination of these factors (P = 0.002). In TT homozygotes, the estimated susceptibility to RA was more than double (OR = 5.04) of that seen in TC heterozygotes (OR = 1.89); the same gene dosage effect was observed in all seropositive RA subgroups. Our data show that the Hungarian RA patients belong to the populations in which the 1858T allele represents a susceptibility factor both in the RF- and/or anti-CCP-seropositive subjects, and the association exhibit a gene dosage dependency.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Rheumatology International. - 29 : 7 (2009), p. 793-796. -
További szerzők:Tálián Gábor Komlósi Katalin Nagy Gergely György (1976-) (orvos) Berki Tímea Gyetvai Ágnes Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Nyárády Zoltán Kiss Csaba György Németh Péter Czirják László Melegh Béla
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001-es BibID:BIBFORM007057
Első szerző:Faragó Bernadett
Cím:Functional variants of interleukin-23 receptor gene confer risk for rheumatoid arthritis but not for systemic sclerosis / Farago, B., Magyari, L., Safrany, E., Csongei, V., Jaromi, L., Horvatovich, K., Sipeky, C., Maasz, A., Radics, J., Gyetvai, A., Szekanecz, Z., Czirjak, L., Melegh, B.
Dátum:2008
ISSN:1468-2060 (Electronic)
Megjegyzések:Recently, an association was found between Crohn's disease and the interleukin-23 receptor (IL-23R) gene. Since the IL-23/IL-17 pathway is known to associate with other autoimmune diseases, including rheumatoid arthritis (RA) and systemic sclerosis (SSc), we hypothesised that IL-23R could be a shared susceptibility gene. METHODS: Groups of patients with rheumatoid arthritis (n = 412), systemic sclerosis (n = 224), Crohn's disease (n = 190) and healthy controls (n = 220) were genotyped for rs10889677 (exon-3'UTR C2370A), rs2201841, and rs1884444 variants; the first two have been shown to confer risk for Crohn's disease. RESULTS: We observed an increased prevalence of the homozygous rs10889677 AA and homozygous rs2201841 CC genotypes both in the Crohn's disease and in the RA groups as compared to the controls (12.1%, 11.9% vs 5.91%, p<0.05; and 13.2%, 13.1% vs 5.91%, p<0.05), but not in the SSc patients. Logistic regression analysis revealed that bearing these alleles represent risk for the development of rheumatoid arthritis (chi(2) = 5.58, p = 0.018, OR = 2.15, 95% CI 1.14-4.06 for rs10889677; and chi(2) = 7.45, p = 0.006, OR = 2.40, 95% CI 1.28-4.51 for rs2201841). The rs1884444 allele, which has been previously reported as neutral for development of Crohn's disease, was also found neutral for all studied groups in the present study. CONCLUSIONS: The data reported here provide direct evidence that some allelic variants or haplogroups of IL-23R represent independent risk factors for rheumatoid arthritis as well as Crohn's disease, but not for scleroderma.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Arthritis, Rheumatoid
Autoantibodies
Crohn Disease
Female
Genetic Predisposition to Disease
Genotype
Humans
Male
Middle Aged
Odds Ratio
Receptors, Interleukin
Scleroderma, Systemic
Megjelenés:Annals of the Rheumatic Diseases. - 67 : 2 (2008), p. 248-250. -
További szerzők:Magyari Lili Sáfrány Enikő Csöngei Veronika Járomi Luca Horvatovich Katalin Sipeky Csilla Maász Anita Radics J. Gyetvai Ágnes Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Czirják László Melegh Béla
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