spondylitis/tyrosine

BACKGROUND Ankylosing spondylitis (AS) is a chronic autoimmune disease that involves the imbalance of peripheral tolerance possibly caused by the negative signal of activated T cells. The polymorphisms in the human protein tyrosine phosphatase non-receptor type 22 (PTPN22) gene have been pointed out

B*2704 and B*2706 are two closely related HLA-B27 subtypes, which differ from the common B*2705 by the Asp > Ser77, Val > Glu152, and Ala > Gly211 amino acid changes. In addition, B*2706 differs from B*2704 by the His > Asp114 and Asp > Tyr116 changes. In spite of their similarity B*2704, but not

BACKGROUND Protein tyrosine phosphatase non-receptor 22 (PTPN22) is a key negative regulator of T lymphocytes and has emerged as an important candidate susceptibility factor for a number of immune-related diseases. This study aimed to examine the predisposition of PTPN22 SNPs to Vogt-Koyanagi-Harada

OBJECTIVE The protein tyrosine phosphatase non-receptor type 22 (PTPN22) is generally accepted as a key factor in maintaining immune cellular homeostasis. So far, no association has been reported between the polymorphisms of PTPN22 and ankylosing spondylitis (AS) in Chinese populations. We attempted

28 plasma amino acids of 40 female patients with rheumatoid arthritis (RA), 24 male patients with ankylosing spondylitis (ASp) and 19 controls (14 females and 5 males) were investigated. In RA-patients 19 amino acids showed statistically significant differences to healthy people of which 18 were

OBJECTIVE Circulating monocytes/macrophages are origins of osteoclasts that mediate the development of ankylosing spondylitis (AS). Moreover, infiltrated macrophages facilitate the AS progression through production and secretion of pro-inflammatory cytokines. Thus, suppression of the recruitment of

Several previous studies have attempted to investigate the regulatory mechanisms underlying gene expression in ankylosing spondylitis (AS). However, the specific molecular pathways underlying this condition remain unclear. Previous research used next-generation RNA sequencing to identify a series of

METHODS A comprehensive bioinformatics analysis of genes which may have correlations with ankylosing spondylitis (AS). OBJECTIVE To study the mechanisms of AS by analyzing microarray of GSE25101. BACKGROUND AS is an inflammatory arthritis that can lead to chronic pain and

OBJECTIVE The present study first utilized a standardized shotgun proteomic analysis method to determine differences in protein expression of fibroblasts in the ligament between AS patients and healthy controls. METHODS Proteins extracted from primarily cultured FLLs from 35 AS patients and 10

This study was designed to identify and quantify the different proteins expression levels in ankylosing spondylitis (AS) and to explore the pathogenesis of AS. We performed isobaric tags for relative and absolute quantitation (iTRAQ) coupled with multiple chromatographic fractionation and tandem

To evaluate the immunomodulating and clinical effects of nilotinib, a tyrosine kinase inhibitor, in a proof-of-concept study in spondyloarthritis (SpA) assessing the mast cell as potential novel therapeutic target in this disease. Twenty eight patients with active peripheral (pSpA) and/or axial SpA

OBJECTIVE To investigate the role of protein tyrosine phosphatase nonreceptor type 2 (PTPN2) in the pathogenesis of rheumatoid arthritis (RA). METHODS Synovial tissue samples from patients with RA and patients with osteoarthritis (OA) were stained for PTPN2. Synovial fibroblasts were stimulated with

Ankylosing spondylitis (AS) is an autoimmune disease, and the imbalance of peripheral tolerance is involved in its pathogenesis. Importantly, the negative signal of activated T cells plays a crucial role in the balance of peripheral tolerance. It has been postulated that human protein tyrosine

OBJECTIVE Interleukin 23 (IL-23) stimulates the differentiation of T helper 17 (Th17) cells, which are involved in the pathogenesis of ankylosing spondylitis (AS). Binding of IL-23 to the IL-23 receptor complex activates Janus kinases 2 and tyrosine kinase 2, which phosphorylate IL-23R and

BACKGROUND IL-17A has recently emerged as a potential target that regulates the extensive inflammation and abnormal bone formation observed in ankylosing spondylitis (AS). Blocking IL-17A is expected to inhibit bony ankylosis. Here, we investigated the effects of anti IL-17A agents in