IL-10 and TNFα Genotypes in SLE

被引:51
作者
Lopez, Patricia [1 ,2 ]
Gutierrez, Carmen [1 ,3 ]
Suarez, Ana [1 ]
机构
[1] Univ Oviedo, Dept Funct Biol, Immunol Area, E-33006 Oviedo, Asturias, Spain
[2] CSIC, Inst Prod Lacteos Asturias, Dept Microbiol & Biochem Dairy Prod, Villaviciosa 33300, Asturias, Spain
[3] Hosp Univ Cent Asturias, Dept Immunol, Oviedo 33006, Asturias, Spain
来源
JOURNAL OF BIOMEDICINE AND BIOTECHNOLOGY | 2010年
关键词
SYSTEMIC-LUPUS-ERYTHEMATOSUS; TUMOR-NECROSIS-FACTOR; INTERLEUKIN-10 PROMOTER POLYMORPHISMS; SINGLE-NUCLEOTIDE POLYMORPHISMS; GAMMA RECEPTOR IIA; GENE POLYMORPHISMS; RHEUMATOID-ARTHRITIS; CYTOKINE PRODUCTION; MICROSATELLITE POLYMORPHISMS; DETERMINING SUSCEPTIBILITY;
D O I
10.1155/2010/838390
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
The production of two regulators of the inflammatory response, interleukin 10 (IL-10) and tumor necrosis factor alpha (TNF alpha), has been found to be deeply deregulated in SLE patients, suggesting that these cytokines may be involved in the pathogenesis of the disease. Genetic polymorphisms at the promoter regions of IL-10 and TNF alpha genes have been associated with different constitutive and induced cytokine production. Given that individual steady-state levels of these molecules may deviate an initial immune response towards different forms of lymphocyte activation, functional genetic variants in their promoters could influence the development of SLE. The present review summarizes the information previously reported about the involvement of IL-10 and TNF alpha genetic variants on SLE appearance, clinical phenotype, and outcome. We show that, in spite of the heterogeneity of the populations studied, the existing knowledge points towards a relevant role of IL-10 and TNF alpha genotypes in SLE.
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页数:11
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