scholarly journals Use of “synovial” cell cultures in the search for virus in rheumatoid arthritis

1965 ◽  
Vol 8 (6) ◽  
pp. 1047-1052 ◽  
Author(s):  
Denys K. Ford ◽  
Jang O. Oh
Autoimmunity ◽  
1991 ◽  
Vol 10 (1) ◽  
pp. 35-39 ◽  
Author(s):  
R. Johnstone ◽  
I. D. Griffiths ◽  
J. E. Calvert

2021 ◽  
Vol 41 (1) ◽  
Author(s):  
Haruka Tsuchiya ◽  
Mineto Ota ◽  
Keishi Fujio

Abstract Background Rheumatoid arthritis (RA) is an autoimmune disease characterized by tumor-like hyperplasia and inflammation of the synovium, which causes synovial cell invasion into the bone and cartilage. In RA pathogenesis, various molecules in effector cells (i.e., immune cells and mesenchymal cells) are dysregulated by genetic and environmental factors. Synovial fibroblasts (SFs), the most abundant resident mesenchymal cells in the synovium, are the major local effectors of the destructive joint inflammation and exert their effects through the pathogenic production of molecules such as interleukin-6. Main body To date, more than 100 RA susceptibility loci have been identified in genome-wide association studies (GWASs), and finding novel therapeutic targets utilizing genome analysis is considered a promising approach because some candidate causal genes identified by GWASs have previously been established as therapeutic targets. For further exploration of RA-responsible cells and cell type-specific therapeutic targets, integrated analysis (or functional genome analysis) of the genome and intermediate traits (e.g., transcriptome and epigenome) is crucial. Conclusion This review builds on the existing knowledge regarding the epigenomic abnormalities in RASFs and discusses the recent advances in single-cell analysis, highlighting the prospects of SFs as targets for safer and more effective therapies against RA.


1989 ◽  
Vol 27 (3-4) ◽  
pp. 448-450 ◽  
Author(s):  
M. L. Watson ◽  
G. P. Lewis ◽  
J. Westwick

2021 ◽  
Vol 12 ◽  
Author(s):  
Sha Wu ◽  
Xiao-Feng Li ◽  
Yuan-Yuan Wu ◽  
Su-Qin Yin ◽  
Cheng Huang ◽  
...  

Rheumatoid arthritis (RA), one of the most common autoimmune diseases, is characterized by immune cell infiltration, fibroblast-like synovial cell hyperproliferation, and cartilage and bone destruction. To date, numerous studies have demonstrated that immune cells are one of the key targets for the treatment of RA. N6-methyladenosine (m6A) is the most common internal modification to eukaryotic mRNA, which is involved in the splicing, stability, export, and degradation of RNA metabolism. m6A methylated-related genes are divided into writers, erasers, and readers, and they are critical for the regulation of cell life. They play a significant role in various biological processes, such as virus replication and cell differentiation by controlling gene expression. Furthermore, a growing number of studies have indicated that m6A is associated with the occurrence of numerous diseases, such as lung cancer, bladder cancer, gastric cancer, acute myeloid leukemia, and hepatocellular carcinoma. In this review, we summarize the history of m6A research and recent progress on RA research concerning m6A enzymes. The relationship between m6A enzymes, immune cells, and RA suggests that m6A modification offers evidence for the pathogenesis of RA, which will help in the development of new therapies for RA.


2021 ◽  
Author(s):  
Søren Lomholt ◽  
Morten A. Nielsen ◽  
Maithri P. Aspari ◽  
Peter B. Jørgensen ◽  
Adam P. Croft ◽  
...  

Fibroblasts like synoviocytes (FLS) play several significant roles in rheumatoid arthritis (RA) pathophysiology. This chapter will describe known roles of FLS in disease initiation, joint inflammation, disease persistence and joint destruction. It will describe the newly characterized subsets of FLS based on single cell RNA sequencing studies, and their association to specific aspects of the disease. Finally, we will discuss the future of targeting FLS in the treatment of RA. The FLS in the synovial lining layer are identified by surface complement decay-accelerating factor (CD55) along with lubricin and metallopeptidase expression. Pathological activation of this lining layer subset result in bone and cartilage damage in mice. FLS of the sublining layer are often characterized by THY1 expression, but recent studies have highlighted a heterogeneity where several distinct subsets are identified by additional markers. Sublining FLS expressing human leukocyte antigen-DRA (HLA-DRA) produce C-X-C motif chemokine 12 (CXCL12) and receptor activator of nuclear factor-κB ligand (RANKL) and seems to constitute a pro-inflammatory subset that is associated with inflammation and tertiary lymphoid structures. Another subset of FLS characterized by CD34 expression may discriminate a common progenitor fibroblast subset. Taken together, studies isolating and characterizing gene expression in synovial FLS report both associations of unknown importance and markers that may impose protective or destructive features. This supports evidence of FLS as active players in RA pathology capable of cellular recruitment, local cellular crosstalk and promotion of joint destruction. These discoveries may serve as an atlas for synovial activation in RA and have identified several potential fibroblast markers for the development of targeted treatment.


2018 ◽  
Vol 70 (7) ◽  
pp. 984-999 ◽  
Author(s):  
Jane Falconer ◽  
Anne N. Murphy ◽  
Stephen P. Young ◽  
Andrew R. Clark ◽  
Stefano Tiziani ◽  
...  

Cytokine ◽  
1990 ◽  
Vol 2 (2) ◽  
pp. 149-155 ◽  
Author(s):  
David H. Goddard ◽  
Scott L. Grossman ◽  
Mary E. Moore

1983 ◽  
Vol 3 (2) ◽  
pp. 125-140 ◽  
Author(s):  
Elaine E. Golds ◽  
T. Derek Cooke ◽  
A. Robin Poole

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