Abstract
Systemic lupus erythematosus (SLE) is a complex multisystem autoimmune disease afflicting more than 600,000 individuals in China. RANTES (regulated on activation, normal T cell expressed and secreted, 17q11.2-q12) is a member of the proinflammatory cytokine family known as “chemokines”. It plays an important role in the attraction and recruitment of lymphocytes, monocytes and eosinophils to sites of inflammation. A total of 146 SLE patients and 159 random healthy volunteer individuals in Han Chinese patients were enrolled in this study. Genotypes of RANTES −403 locus and −28 locus were observed to be different in all racial groups. The frequency of individuals who possessed G allele at −28 locus among SLE patients was not significantly different from that among normal controls. A total of seven compound genotypes at −403 locus and −28 locus were observed in this study. The frequency of this compound genotype (−403 G/G, −28 C/C) was different between the two groups. The distribution of genotypes and alleles at RANTES-403 locus was observed to be significantly different between renal damaged group and no renal damaged group (P<0.05), while there was no significant difference in distribution of genotypes and alleles at RANTES-28 locus between the two groups. These results suggest that (a) two genetic polymorphisms in the RANTES promoter do not correlate with SLE as individual polymorphisms. (b) interaction of the polymorphisms at two loci probably exerts a risk effect against SLE and (c) polymorphism at RANTES-403 locus is probably related with renal damage.
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Acknowledgements
We thank the patients for their cooperation in donating blood samples. This work was funded by grants from the National Natural Science Foundation of China (30371247), the Natural Science Foundation of Anhui Province (98437231) and the Key Program of Anhui Province Education Department (2002 kj175ZD).
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Ye, D.Q., Yang, S.G., Li, X.P. et al. Polymorphisms in the promoter region of RANTES in Han Chinese and their relationship with systemic lupus erythematosus. Arch Dermatol Res 297, 108–113 (2005). https://doi.org/10.1007/s00403-005-0581-9
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DOI: https://doi.org/10.1007/s00403-005-0581-9