ArticleThe Journal of clinical investigation2001
Rheumatoid arthritis synovial T cells regulate transcription of several genes associated with antigen-induced anergy.
Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 45 citations in OpenAlex.
- Role of cytokine in malignant T-cell metabolism and subsequent alternation in T-cell tumor microenvironment.Frontiers in oncology · 2023Review
- Control of T Cell Metabolism by Cytokines and Hormones.Frontiers in immunology · 2021Review
- Review
- Modulation of peripheral T-cell function by interleukin-7 in rheumatoid arthritis.Arthritis research & therapy · 2014Article
- Gene expression analysis in RA: towards personalized medicine.The pharmacogenomics journal · 2014Review
- TNFα promotes Th17 cell differentiation through IL-6 and IL-1β produced by monocytes in rheumatoid arthritis.Journal of immunology research · 2014Article
- Phosphorylation of FOXP3 controls regulatory T cell function and is inhibited by TNF-α in rheumatoid arthritis.Nature medicine · 2013Article
- Article
- Combination of nifedipine and subtherapeutic dose of cyclosporin additively suppresses mononuclear cells activation of patients with rheumatoid arthritis and normal individuals via Ca(2+) -calcineurin-nuclear factor of activated T cells pathway.Clinical and experimental immunology · 2012Article
- NSAIDS inhibit in vitro MSC chondrogenesis but not osteogenesis: implications for mechanism of bone formation inhibition in man.Journal of cellular and molecular medicine · 2011Article
- High frequency of nonrecurrent MECP2 duplications among Brazilian males with mental retardation.Journal of molecular neuroscience : MN · 2010Article
- Altered microRNA expression profile with miR-146a upregulation in CD4+ T cells from patients with rheumatoid arthritis.Arthritis research & therapy · 2010Article
- Effects of decreased calmodulin protein on the survival mechanisms of alveolar macrophages during Pneumocystis pneumonia.Infection and immunity · 2009Article
- Impaired bone marrow hematopoietic progenitor cell function in rheumatoid arthritis patients candidated to autologous hematopoietic stem cell transplantation.Bone marrow transplantation · 2004Article
- Antigen-specific T cells in rheumatoid arthritis.Current rheumatology reports · 2003Review
- Studies of T-cell activation in chronic inflammation.Arthritis research · 2002Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Rheumatoid arthritis (RA) is a chronic, inflammatory synovitis whose pathogenesis may involve autoimmune mechanisms. Anergy is a state of T-cell nonresponsiveness characterized by downregulated IL-2 production. Paradoxically, RA T cells are hyporesponsive and proliferate poorly to antigens and mitogens, thus sharing some characteristics with anergic T cells. We analyzed the molecular basis of anergy in cloned human CD4+ T cells using differential display RT-PCR and subsequently examined the levels of differentially expressed transcripts in RA and, as control, reactive arthritis (ReA) synovium. Several transcriptional events were common to anergic T cells and RA synovium. These included downregulation of CALMODULIN:, which is critical to T-cell activation, and of cellular apoptosis susceptibility protein, which may mediate resistance to apoptosis in RA. Transcription of CALMODULIN: in RA synovium was less than 1% of that in ReA and was lower in RA synovial fluid mononuclear cells than in paired PBMCs. Following anti-TNF-alpha therapy in vivo, RA PBMC CALMODULIN: transcripts increased five- to tenfold. Pharmacological calmodulin blockade in vitro impaired antigen-specific proliferation. These data provide a link between reduced CALMODULIN: transcription and impaired T-cell responsiveness in RA. The identification of transcriptional changes common to anergic and RA synovial T cells should help interpret some of the characteristic RA cellular defects.
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