The chicken MHC YF1*7.1 X-ray structures reveal that this protein binds lipids and thus represents a "hybrid" class I complex with features of classical as well as non-classical MHC molecules.
YF1*7.1 is an allele of a polymorphic major histocompatibility complex (MHC) class I‐like locus within the chicken Y gene complex. With the aim of understanding the possible role of the YF1*7.1 molecule in antigen presentation, the complex of YF1*7.1 heavy chain and β2‐microglobulin was reconstituted and purified without a peptide. Crystals diffracted synchrotron radiation to 1.32 Å resolution and belonged to the monoclinic space group P21. The phase problem was solved by molecular replacement. A detailed examination of the structure may provide insight into the type of ligand that could be bound by the YF1*7.1 molecule.
Aim: Recent studies have shown that single nucleotide polymorphisms (SNPs) have been identified within the promoter of the human interleukin‐10 (IL‐10) gene may participate in the pathogenesis of systemic lupus erythematosus (SLE) and may be related to disease activity. This is a pilot study that investigated the allelic and genotype frequencies of three SNPs in the human IL‐10 gene promoter [rs1800896 (position: –1082G > A), rs1800871 (position: –824C > T) and rs1800872 (position: –597C > A)] among Malaysian SLE patients and normal subjects.
Methods: Blood was drawn from 44 SLE patients and 44 age‐ and sex‐matched healthy control subjects for DNA extraction. The SNPs were identified using the polymerase chain reaction‐restriction fragment length polymorphism (PCR‐RFLP) method.
Results: There was no significant difference in the genotype and allele frequencies between the SLE patients and control subjects. A statistically significant difference was detected in the haplotype frequencies between the patients and controls (P = 0.004).
Conclusions: There is a significant difference in the haplotype frequencies between the SLE patients and controls; the SNPs in the human IL‐10 gene promoter could play an important role in the pathogenesis of SLE.
In this study, three single nucleotide polymorphisms (SNPs) located within the promoter of the human interleukin (IL)-10 gene [rs1800896 (position: -1087G>A), rs1800871 (position: -824C>T) and rs1800872 (position: -597C>A)] were investigated in 84 rheumatoid arthritis (RA) patients and 95 age- and sex-matched healthy subjects using polymerase chain reaction-restriction fragment length polymorphism method. Production of IL-10 by peripheral blood lymphocytes from the RA patients and healthy subjects cultured in the presence of Concanavalin A (Con A) was determined by using enzyme-linked immunosorbent assay. The results show that the distribution of the IL-10 genotypes did not differ significantly between RA patients and healthy subjects (P>0.05). However, a significant difference was observed in allele frequencies of -824CT, -824TT, -597CA, and -597AA between the RA patients and healthy volunteers (P=0.04). The -1087A/-824T/-597A (ATA) haplotype, which comprises all mutant alleles, was associated with lower IL-10 production when compared with the other haplotypes. In contrast, the RA patients who did not display the ATA haplotype produced significantly higher levels of IL-10 when compared with those carrying either one (P=0.012) or two (P=0.005) ATA haplotypes. Our findings suggest that there is an association between SNPs in the promoter of the human IL-10 gene and susceptibility to RA.
In this study, three single nucleotide polymorphisms (SNPs) located within the promoter of the human interleukin (IL)-10 gene [rs1800896 (position: -1087G>A), rs1800871 (position: -824C>T) and rs1800872 (position: -597C>A)] were investigated in 84 rheumatoid arthritis (RA) patients and 95 age- and sex-matched healthy subjects using polymerase chain reaction-restriction fragment length polymorphism method. Production of IL-10 by peripheral blood lymphocytes from the RA patients and healthy subjects cultured in the presence of Concanavalin A (Con A) was determined by using enzyme-linked immunosorbent assay. The results show that the distribution of the IL-10 genotypes did not differ significantly between RA patients and healthy subjects (P>0.05). However, a significant difference was observed in allele frequencies of -824CT, -824TT, -597CA, and -597AA between the RA patients and healthy volunteers (P=0.04). The -1087A/-824T/-597A (ATA) haplotype, which comprises all mutant alleles, was associated with lower IL-10 production when compared with the other haplotypes. In contrast, the RA patients who did not display the ATA haplotype produced significantly higher levels of IL-10 when compared with those carrying either one (P=0.012) or two (P=0.005) ATA haplotypes. Our findings suggest that there is an association between SNPs in the promoter of the human IL-10 gene and susceptibility to RA.
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