Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: A polymorphism in the interleukin-4 receptor affects the ability of interleukin-4 to regulate Th17 cells: a possible immunoregulatory mechanism for genetic control of the severity of rheumatoid arthritis. | Wallis et al. Arthritis Research Therapy 2011 13 R15 http content 13 1 R15 RESEARCH ARTICLE Open Access A polymorphism in the interleukin-4 receptor affects the ability of interleukin-4 to regulate Th17 cells a possible immunoregulatory mechanism for genetic control of the severity of rheumatoid arthritis Susan K Wallis Laura A Cooney Judith L Endres Min Jie Lee Jennifer Ryu Emily C Somers David A Fox Abstract Introduction Rheumatoid arthritis RA is now suspected to be driven by pathogenic Th17 cells that secrete interleukin IL -17 and can be regulated by IL-4. A single-nucleotide polymorphism SNP I50V in the coding region of the human IL-4 receptor IL-4R is associated with rapid development of erosive disease in RA. The present study was undertaken to determine whether this SNP renders the IL-4R less able to transduce signals that regulate IL-17 production. Methods Peripheral blood mononuclear cells were activated under Th17-stimulating conditions in the presence or absence of IL-4 and IL-17 production was measured by both enzyme-linked immunosorbent assay ELISA and flow cytometry. Serum IL-17 was also measured by ELISA. Paired comparisons were performed using the two-tailed t-test. IL-4 receptor gene alleles were determined by polymerase chain reaction. Results In healthy individuals IL-4 significantly inhibited IL-17 production by cells from subjects with the I I genotype P and the I V genotype P but not the V V genotype P . In a cross-sectional sample of patients with established RA the magnitude of the in vitro effect of IL-4 was lower and was not associated with a specific IL-4R allele. Serum IL-17 levels were higher in RA patients than in healthy individuals as was the percentage of CD4 cells that produced IL-17. Conclusions These results indicate that an inherited polymorphism of the IL-4R controls the ability of the human immune system to regulate the magnitude of IL-17 production. However in established RA this .
