共查询到20条相似文献,搜索用时 31 毫秒
1.
Bianca Miterski Susanne Drynda Gundula B?schow Wolfram Klein Joachim Oppermann J?rn Kekow J?rg Thomas Epplen 《BMC genetics》2004,5(1):2
Background
Rheumatoid arthritis (RA) and juvenile rheumatoid arthritis (JRA) are complex multifactorial diseases caused by environmental influences and an unknown number of predisposing genes. The present study was undertaken in order to investigate association of polymorphisms in candidate genes with RA and JRA in German subjects. 相似文献2.
Klaus Stark Jozef Rovenský Stanislava Blažičková Hans Grosse-Wilde Stanislav Ferencik Christian Hengstenberg Rainer H Straub 《Arthritis research & therapy》2009,11(3):R70-10
Introduction
Both genetic and environmental factors contribute to rheumatoid arthritis (RA), a common and complex autoimmune disease. As well as the major susceptibility gene HLA-DRB1, recent genome-wide and candidate-gene studies reported additional evidence for association of single nucleotide polymorphism (SNP) markers in the PTPN22, STAT4, OLIG3/TNFAIP3 and TRAF1/C5 loci with RA. This study was initiated to investigate the association between defined genetic markers and RA in a Slovak population. In contrast to recent studies, we included intensively-characterized osteoarthritis (OA) patients as controls. 相似文献3.
Nielsen KR Steffensen R Boegsted M Baech J Lundbye-Christensen S Hetland ML Krintel SB Johnsen HE Nyegaard M Johansen JS 《Arthritis research & therapy》2011,13(3):R109
Introduction
The present study investigates the association between single nucleotide polymorphisms (SNPs) in the chitinase 3-like 1 (CHI3L1) gene and serum concentrations of YKL-40 in Danish patients with rheumatoid arthritis (RA) and healthy controls as well as the association with RA in the Danish population. The CHI3L1 gene is located on chromosome 1q32.1 and encodes the YKL-40 glycoprotein. YKL-40 concentrations are elevated in the serum of patients with RA compared to healthy subjects, and YKL-40 has been suggested to be an auto-antigen and may play a role in development of RA and in inflammation. 相似文献4.
Barnetche T Constantin A Cantagrel A Cambon-Thomsen A Gourraud PA 《Arthritis research & therapy》2008,10(1):R26
Introduction
Rheumatoid arthritis (RA) is a complex polygenic disease of unknown etiology. HLA-DRB1 alleles encoding the shared epitope (SE) (RAA amino acid pattern in positions 72 to 74 of the third hypervariable region of the DRβ1 chain) are associated with RA susceptibility. A new classification of HLA-DRB1 SE alleles has been developed by Tezenas du Montcel and colleagues to refine the association between HLA-DRB1 and RA. In the present study, we used RA samples collected worldwide to investigate the relevance of this new HLA-DRB1 classification in terms of RA susceptibility across various Caucasoid and non-Caucasoid patients. 相似文献5.
Rogelio Palomino-Morales Carlos Gonzalez-Juanatey Tomas R Vazquez-Rodriguez Luis Rodriguez Jose A Miranda-Filloy Benjamin Fernandez-Gutierrez Javier Llorca Javier Martin Miguel A Gonzalez-Gay 《Arthritis research & therapy》2010,12(2):R71
Introduction
We determined the contribution of the methylene tetrahydrofolate reductase (MTHFR) 677 C>T and 1298 A>C gene polymorphisms to the susceptibility to rheumatoid arthritis (RA). We also assessed whether these two MTHFR gene polymorphisms may be implicated in the development of cardiovascular (CV) events and subclinical atherosclerosis manifested by the presence of endothelial dysfunction, in a series of Spanish patients with RA. 相似文献6.
Huber R Hummert C Gausmann U Pohlers D Koczan D Guthke R Kinne RW 《Arthritis research & therapy》2008,10(4):R98
Introduction
Rheumatoid arthritis (RA) is a chronic inflammatory and destructive joint disease characterized by overexpression of pro-inflammatory/pro-destructive genes and other activating genes (for example, proto-oncogenes) in the synovial membrane (SM). The gene expression in disease is often characterized by significant inter-individual variances via specific synchronization/desynchronization of gene expression. To elucidate the contribution of the variance to the pathogenesis of disease, expression variances were tested in SM samples of RA patients, osteoarthritis (OA) patients, and normal controls (NCs). 相似文献7.
Ioanna Marinou Simon H Till David J Moore Anthony G Wilson 《Arthritis research & therapy》2008,10(4):R80
Introduction
A feature of rheumatoid arthritis (RA) is an imbalance between proinflammatory and anti-inflammatory cytokines. Several recent studies have implicated polymorphism in the IL-4 signalling pathway in the development of erosive RA. The aim of the present study was to investigate the role of polymorphism in the IL-4, IL-4Rα and IL-13 genes in RA, including an examination of epistasis. 相似文献8.
Saevarsdottir S Ding B Steinsson K Grondal G Valdimarsson H Alfredsson L Klareskog L Padyukov L 《Arthritis research & therapy》2011,13(2):R65
Introduction
Previous studies have provided inconsistent results on whether variants in the MBL2 gene, coding for the complement-activating mannan-binding lectin (MBL) protein, associate with rheumatoid arthritis (RA). We re-evaluated this in context of the main environmental and genetic risk factors (smoking, HLA-DRB1 'shared epitope' (SE), PTPN22*620W), which predispose to rheumatoid factor (RF) and/or anti-citrullinated-protein antibody (ACPA)-positive RA. 相似文献9.
Kristin Andreas Thomas Häupl Carsten Lübke Jochen Ringe Lars Morawietz Anja Wachtel Michael Sittinger Christian Kaps 《Arthritis research & therapy》2009,11(1):R15-14
Introduction
Rheumatoid arthritis (RA) leads to progressive destruction of articular cartilage. This study aimed to disclose major mechanisms of antirheumatic drug action on human chondrocytes and to reveal marker and pharmacological target genes that are involved in cartilage dysfunction and regeneration. 相似文献10.
So-Young Bang Tae-Un Han Chan-Bum Choi Yoon-Kyoung Sung Sang-Cheol Bae Changwon Kang 《Arthritis research & therapy》2010,12(3):R115
Introduction
Anti-cyclic citrullinated peptide autoantibodies (anti-CCP) are the most specific serologic marker for rheumatoid arthritis (RA). Genetic polymorphisms in a citrullinating (or deiminating) enzyme, peptidyl arginine deiminase type IV (PADI4) have been reproducibly associated with RA susceptibility in several populations. We investigated whether PADI4 polymorphisms contribute to anti-CCP-negative as well as -positive RA, whether they influence disease severity (erosive joint status), and whether they interact with two major risk factors for RA, Human Leukocyte Antigen-DRB1 (HLA-DRB1) shared epitope (SE) alleles and smoking, depending on anti-CCP and erosive joint status. 相似文献11.
Introduction
In a murine model, interleukin (IL)-17 plays a critical role in the pathogenesis of arthritis. There are controversies, however, regarding whether IL-17 is a proinflammatory mediator in rheumatoid arthritis (RA). We previously established an ex vivo cellular model using synovial tissue (ST)-derived inflammatory cells, which reproduced pannus-like tissue growth and osteoclastic activity in vitro. Using this model, we investigated the effects of IL-17 on pannus growth and osteoclastogenesis in RA. 相似文献12.
Scott W Graf Sue Lester Johannes C Nossent Catherine L Hill Susanna M Proudman Anita Lee Maureen Rischmueller 《Arthritis research & therapy》2012,14(1):R28-7
Introduction
Low copy number (CN) of the Fc gamma receptor 3B (FCGR3B) gene has been associated with systemic autoimmune disease. This receptor for IgG is present almost exclusively on neutrophils and plays a role in their interaction with immune complexes. At present the relationship between FCGR3B and rheumatoid arthritis (RA) is unclear. The aim of the present study was to investigate whether low CN of the FCGR3B gene is associated with susceptibility to RA. 相似文献13.
Chung SH Seki K Choi BI Kimura KB Ito A Fujikado N Saijo S Iwakura Y 《Arthritis research & therapy》2010,12(5):R188
Introduction
Chemokines and their receptors are potential therapeutic targets in rheumatoid arthritis (RA). Among these, several studies suggested the involvement of CXC chemokine 4 (CXCR4) and its ligand CXC ligand 12 (SDF-1) in RA pathogenesis. However, the role of these molecules in T-cell function is not known completely because of embryonic lethality of Cxcr4- and Cxcl12- deficient mice. In this report, we generated T cell-specific Cxcr4 -deficient mice and showed that the CXCR4 in T cells is important for the development of collagen-induced arthritis (CIA). 相似文献14.
Jessica AB van Nies Rute B Marques Stella Trompet Zuzana de Jong Fina AS Kurreeman Rene EM Toes J Wouter Jukema Tom WJ Huizinga Annette HM van der Helm-van Mil 《Arthritis research & therapy》2010,12(2):R38
Introduction
Recently an association between a genetic variation in TRAF1/C5 and mortality from sepsis or cancer was found in rheumatoid arthritis (RA). The most prevalent cause of death, cardiovascular disease, may have been missed in that study, since patients were enrolled at an advanced disease stage. Therefore, we used an inception cohort of RA patients to investigate the association between TRAF1/C5 and cardiovascular mortality, and replicate the findings on all-cause mortality. As TRAF1/C5 associated mortality may not be restricted to RA, we also studied a large cohort of non-RA patients. 相似文献15.
de Groot L Hinkema H Westra J Smit AJ Kallenberg CG Bijl M Posthumus MD 《Arthritis research & therapy》2011,13(6):R205
Introduction
Advanced glycation end products (AGEs) are produced and can accumulate during chronic inflammation, as might be present in patients with rheumatoid arthritis (RA). AGEs are involved in the development of cardiovascular disease. The aim of this study is to evaluate whether AGEs are increased in patients with long-standing RA and whether AGE accumulation is related to disease activity, disease severity and measures of (premature) atherosclerosis, such as endothelial activation, endothelial dysfunction and intima media thickness (IMT). 相似文献16.
Rodríguez-Rodríguez L González-Juanatey C García-Bermúdez M Vázquez-Rodríguez TR Miranda-Filloy JA Fernández-Gutiérrez B Llorca J Martin J González-Gay MA 《Arthritis research & therapy》2011,13(4):R133
Introduction
The aim of our study was to analyze the influence of the CCR5Δ32 polymorphism in the risk of cardiovascular (CV) events and subclinical atherosclerosis among patients with rheumatoid arthritis (RA). 相似文献17.
Shoko Toyama Naoto Tamura Kazuhiko Haruta Takeo Karakida Shigeyuki Mori Tetsuo Watanabe Takao Yamori Yoshinari Takasaki 《Arthritis research & therapy》2010,12(3):R92
Introduction
Targeting joint destruction induced by osteoclasts (OCs) is critical for management of patients with rheumatoid arthritis (RA). Since phosphoinositide 3-kinase (PI3-K) plays a critical role in osteoclastogenesis and bone resorption, we examined the effects of ZSTK474, a novel phosphoinositide 3-kinase (PI3-K)-specific inhibitor, on murine OCs in vitro and in vivo. 相似文献18.
Manon JM van Oosten Radboud JEM Dolhain Jan W Koper Elisabeth FC van Rossum Marieke Emonts Khik H Han Jacques MGW Wouters Johanne MW Hazes Steven WJ Lamberts Richard A Feelders 《Arthritis research & therapy》2010,12(4):R159
Introduction
The glucocorticoid receptor (GR) plays an important regulatory role in the immune system. Four polymorphisms in the GR gene are associated with differences in glucocorticoid (GC) sensitivity; the minor alleles of the polymorphisms N363 S and BclI are associated with relative hypersensitivity to GCs, while those of the polymorphisms ER22/23EK and 9β are associated with relative GC resistance. Because differences in GC sensitivity may influence immune effector functions, we examined whether these polymorphisms are associated with the susceptibility to develop Rheumatoid Arthritis (RA) and RA disease severity. 相似文献19.
Gompels LL Malik NM Madden L Jin P Feldmann M Shepard HM Paleolog EM 《Arthritis research & therapy》2011,13(5):R161
Introduction
Rheumatoid arthritis (RA) is a chronic disease associated with inflammation and destruction of bone and cartilage. Although inhibition of TNFα is widely used to treat RA, a significant number of patients do not respond to TNFα blockade, and therefore there is a compelling need to continue to identify alternative therapeutic strategies for treating chronic inflammatory diseases such as RA. The anti-epidermal growth factor (anti-EGF) receptor antibody trastuzumab has revolutionised the treatment of patients with EGF receptor-positive breast cancer. Expression of EGF ligands and receptors (known as HER) has also been documented in RA. The highly unique compound RB200 is a bispecific ligand trap that is composed of full-length extracellular domains of HER1 and HER3 EGF receptors. Because of its pan-HER specificity, RB200 inhibits responses mediated by HER1, HER2 and HER3 in vitro and in vivo. The objective of this study was to assess the effect of RB200 combined with TNF blockade in a murine collagen-induced arthritis (CIA) model of RA. 相似文献20.
So-Young Bang Young-Ji Na Kwangwoo Kim Young Bin Joo Youngho Park Jaemoon Lee Sun-Young Lee Adnan A Ansari Junghee Jung Hwanseok Rhee Jong-Young Lee Bok-Ghee Han Sung-Min Ahn Sungho Won Hye-Soon Lee Sang-Cheol Bae 《Arthritis research & therapy》2014,16(5)