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| Content Provider | PubMed Central |
|---|---|
| Author | Liu, Cuiping Jiang, Juean Gao, Li Hu, Xiaohan Wang, Fengming Shen, Yu Yu, Gehua Zhao, Zuotao Zhang, Xueguang |
| Copyright Year | 2014 |
| Abstract | Objective. Programmed cell death 1 (PD-1) induces negative signals to T cells during interaction with its ligands and is therefore a candidate gene in the development of autoimmune diseases such as rheumatoid arthritis (RA). Herein, we investigate the association of PDCD-1 polymorphisms with the risk of RA among Chinese patients and healthy controls. Methods. Using the PCR-direct sequencing analysis, 4 PDCD-1 SNPs (rs36084323, rs11568821, rs2227982, and rs2227981) were genotyped in 320 RA patients and 309 matched healthy controls. Expression of PD-1 was determined in peripheral blood lymphocytes by flow cytometry and quantitative real-time reverse transcriptase polymerase chain reaction. Results. We observed that the GG genotype of rs36084323 was associated with a increased risk for developing RA (OR 1.70, 95% 1.11–2.61, P = 0.049). Patients carrying G/G genotype displayed an increased mRNA level of PD-1 (P = 0.04) compared with A/A genotype and healthy controls. Meanwhile, patients homozygous for rs36084323 had induced basal PD-1 expression on activated CD4+ T cells. Conclusion. The PDCD-1 polymorphism rs36084323 was significantly associated with RA risk in Han Chinese population. This SNP, which effectively influenced the expression of PD-1, may be a biomarker of early diagnosis of RA and a suitable indicator of utilizing PD-1 inhibitor for treatment of RA. |
| Related Links | http://dx.doi.org/10.1155/2014/247637 |
| Starting Page | 247637 |
| File Format | |
| ISSN | 2314436X |
| e-ISSN | 23144378 |
| Journal | International Journal of Genomics |
| Volume Number | 2014 |
| Language | English |
| Publisher | Hindawi Publishing Corporation |
| Publisher Date | 2014-01-01 |
| Access Restriction | Open |
| Rights Holder | Hindawi Publishing Corporation |
| Subject Keyword | Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Genetics Molecular Biology Biochemistry Pharmaceutical Science |
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