Upregulated PD-1 Expression Is Associated with the Development of Systemic Lupus Erythematosus, but Not the PD-1.1 Allele of the PDCD1 Gene.
Upregulated PD-1 Expression Is Associated with the Development of Systemic Lupus Erythematosus, but Not the PD-1.1 Allele of the PDCD1 Gene.
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PD-1 表达上调与系统性红斑狼疮的发生有关,但与 PDCD1 基因的 PD-1.1 等位基因无关
DOI:
10.1155/2014/950903
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发表时间:
2014
影响因子:
2.9
通讯作者:
Qian Q
中科院分区:
文献类型:
--
作者:
Jiao Q;Liu C;Yang Z;Ding Q;Wang M;Li M;Zhu T;Qian H;Li W;Tu N;Fang F;Ye L;Zhao Z;Qian Q
Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with complicated genetic inheritance. Programmed death 1 (PD-1), a negative T cell regulator to maintain peripheral tolerance, induces negative signals to T cells during interaction with its ligands and is therefore a candidate gene in the development of SLE. In order to examine whether expression levels of PD-1 contribute to the pathogenesis of SLE, 30 patients with SLE and 30 controls were recruited and their PD-1 expression levels in peripheral blood mononuclear cells (PBMCs) were measured via flow cytometry and quantitative real-time-reverse transcription polymerase chain reaction (RT-PCR). Also, whether PD-1 expression levels are associated with the variant of the SNP rs36084323 and the SLE Disease Activity Index (SLEDAI) was studied in this work. The PD-1 expression levels of SLE patients were significantly increased compared with those of the healthy controls. The upregulated PD-1 expression levels in SLE patients were greatly associated with SLEDAI scores. No significant difference was found between PD-1 expression levels and SNP rs36084323. The results suggest that increased expression of PD-1 may correlate with the pathogenesis of SLE, upregulated PD-1 expression may be a biomarker for SLE diagnosis, and PD-1 inhibitor may be useful to SLE treatment.
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影响因子:
--
作者:
Prokunina, L;Padyukov, L;Alarcón-Riquelme, M
通讯作者:
Alarcón-Riquelme, M
影响因子:
3.5
作者:
Okazaki, T;Wang, P
通讯作者:
Wang, P
影响因子:
4
作者:
Ming, Z. J.;Hui, H.;Zhang, X. G.
通讯作者:
Zhang, X. G.
影响因子:
32.4
作者:
Nishimura, H;Nose, M;Honjo, T
通讯作者:
Honjo, T
影响因子:
--
作者:
BOMBARDIER, C;GLADMAN, DD;CHANG, CH
通讯作者:
CHANG, CH