原创力文档reduction of cartilage destruction in a rapid progressive arthritis model in scid mice减少软骨破坏的快速进步在scid小鼠关节炎模型.pdfVIP
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reduction of cartilage destruction in a rapid progressive arthritis model in scid mice减少软骨破坏的快速进步在scid小鼠关节炎模型
Chang et al. Arthritis Research Therapy 2014, 16:R14
/content/16/1/R14
RESEARCH ARTICLE Open Access
Altered expression of protein tyrosine
phosphatase, non-receptor type 22 isoforms in
systemic lupus erythematosus
1,2 1 1,2 1,2 1,2,3*
Hui-Hsin Chang , William Tseng , Jing Cui , Karen Costenbader and I-Cheng Ho
Abstract
Introduction: A C-to-T single nucleotide polymorphism (SNP) located at position 1858 of human protein tyrosine
phosphatase, non-receptor type 22 (PTPN22) complementary DNA (cDNA) is associated with an increased risk of
systemic lupus erythematosus (SLE). How the overall activity of PTPN22 is regulated and how the expression of
PTPN22 differs between healthy individuals and patients with lupus are poorly understood. Our objectives were to
identify novel alternatively spliced forms of PTPN22 and to examine the expression of PTPN22 isoforms in healthy
donors and patients with lupus.
Methods: Various human PTPN22 isoforms were identified from the GenBank database or amplified directly from
human T cells. The expression of these isoforms in primary T cells and macrophages was examined with real-time
polymerase chain reaction. The function of the isoforms was determined with luciferase assays. Blood samples were
collected from 49 subjects with SLE and 15 healthy controls. Correlation between the level of PTPN22 isoforms in
peripheral blood and clinical features of SLE was examined with statistical analyses.
Results: Human PTPN22 was expressed in several isoforms, which differed in their level of expression and
subcellular localization. All isoforms except one were functionally interchangeable in regulating NFAT activity. SLE
patients expressed higher levels of PTPN22 than healthy individuals an
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