RESUMEN
The aim of this study was to examine the association between polymorphisms in the interleukin-3 and -13 (IL-3 and IL-13) genes and rheumatoid arthritis (RA). In this hospital-based case-control study, we analyzed the IL-3 rs2073506 G/A, IL-3 rs40401 C/T, and IL-13 rs1800925 C/T polymorphisms in 615 RA patients and 839 controls from a Chinese Han population. Genotyping was performed using a custom-by-design 48-Plex single nucleotide polymorphism scanTM kit. Our results indicated that the IL-3 rs2073506 G/A, IL-3 rs40401 C/T, and IL-13 rs1800925 C/T polymorphisms were not associated with RA. However, stratification analyses suggested that the IL-13 rs1800925 CT and CT/CC genotypes increased the risk of RA in patients with erythrocyte sedimentation rate (ESR) <25.00. To sum up, these findings suggest that the IL-13 rs1800925 C/T polymorphism may be associated with increased risk of RA in ESR <25.00 patients. Future studies with larger sample sizes and inclusion of other ethnic populations must be conducted to confirm the findings of this study.
Asunto(s)
Artritis Reumatoide/genética , Predisposición Genética a la Enfermedad , Interleucina-13/genética , Interleucina-3/genética , Anciano , Alelos , Artritis Reumatoide/sangre , Artritis Reumatoide/patología , Sedimentación Sanguínea , Femenino , Estudios de Asociación Genética , Genotipo , Humanos , Masculino , Persona de Mediana Edad , Polimorfismo de Nucleótido SimpleRESUMEN
Coilia mystus is the most important harvested fish species in China; it inhabits quite different water environments during the different life history stages. Populations of C. mystus have dropped sharply due to overharvesting and water pollution. We developed eight microsatellite loci in C. mystus for conservation genetics studies. These new markers were tested in 20 individuals from the Min River in ChangLe. The number of alleles ranged from 3 to 8, the expected heterozygosity from 0.621 to 0.853 and the observed heterozygosity from 0.473-0.800. Only two loci deviated significantly from Hardy-Weinberg expectations due to heterozygote deficiency. These primers may provide a tool for understanding demography and population structure of this economically important and threatened species.
Asunto(s)
Peces/genética , Repeticiones de Microsatélite/genética , Reacción en Cadena de la Polimerasa/métodos , Animales , Técnica del ADN Polimorfo Amplificado AleatorioRESUMEN
In the mouse model, the arbovirus Venezuelan equine encephalitis virus (VEE) replicates in lymphoid tissues prior to either inducing protective immunity (attenuated VEE mutant) or progressing to lethal encephalitis (virulent parent VEE). To investigate the mechanism of the protective response, cytokine gene expression was examined during the course of the primary in vivo immune response to molecularly cloned, virulent VEE and a single-site attenuated VEE mutant, using a quantitative reverse transcriptase-polymerase chain reaction assay. VEE-induced cytokine gene expression was 100-fold elevated over that of untreated controls for IFN-gamma and IL-6 and 10-fold increased for IL-12, IL-10, and TNF-alpha. There was no qualitative difference in cytokine gene induction comparing mice infected with the attenuated and the virulent VEE; however, there were significant differences in the cytokine gene expression kinetics. In mice infected with the attenuated VEE, elevated cytokine gene expression was delayed 24 hr when compared to mice infected with the virulent parent VEE clone at the same dose. Further, IFN-gamma protein secretion by cells from the draining lymph node mimicked the pattern of IFN-gamma gene induction by cells harvested from the same site. IFN-gamma gene expression was elevated at an earlier time point in mice given virulent V3000 24 hr after attenuated V3032 injection compared to mice infected with virulent V3000 alone. The combined V3000/V3032 infection resulted in host protection. Treatment of mice with IL-12 prior to infection with virulent VEE failed to reduce the severity of infection, while anti-IL-12 antibody did not prevent the early protective effect of attenuated virus. In contrast, administration of anti-IFN-alpha/beta antibody prior to VEE infection worsened virulent VEE disease. These results indicate that the attenuated VEE strain elicits a similar but delayed cytokine response compared to the virulent strain, suggesting that the kinetics of cytokine expression and the particular cytokine produced may influence the development of a host protective response. Furthermore, IFN-alpha/beta, but not IL-12, seems to be a major factor in the induction of early protection against VEE infection and disease.