Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Synovial fibroblast cell strains derived from the synovial membranes of 7 patients with rheumatoid arthritis were examined for the presence of viruses, in particular leucoviruses. Seven similar synovial strains derived from patients with other arthritic conditions were used as a control group. Evidence of the presence of a virus or a viral genome was looked for by several methods of induction followed by 3H-uridine labelling of the cultures. In addition, the culture supernatant, after induction and after the synovial strains had been co-cultivated with a variety of cell lines from several species, was assayed for the presence of viral RNA-dependent DNA polymerase activity. The DNA-polymerase activity of the synovial cells themselves was also determined. No evidence was found by any of these techniques to indicate the presence of virus or viral information within the synovial fibroblasts.
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PMID:Attempts to identify viruses in rheumatoid synovial cells. 6 87

Cultured synovial cells from 8 patients with rheumatoid arthritis (RA) and 7 subjects without joint disease were assayed and comapred for RNA-directed and DNA-directed DNA polymerase activity. No activity was found in either RA or control specimens using a synthetic RNA template that specificically detects oncornavirus RNA-directed DNA polymerase. The DNA-directed DNA polymerase activity of RA specimens was increased (P less than 0.10) in the high-speed pellet fraction of cell lysates. The possible relationship of these finding to virus infection in RA is disscussed.
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PMID:DNA polymerase activity of cultured rheumatoid synovial cells. 16 46

Synovial fluid lymphocytes from patients with rheumatoid arthritis have been examined for evidence of a productive infection with retroviruses by electron microscopy, labelling with 3H-uredine, growth in soft agar, and culturing in conditioned medium. No such viruses were detected. In addition, the synovial lymphocytes were activated before fusion and cocultivation with several cell lines which have proved permissive for primate retroviruses. Monitoring these cultures subsequently by reverse transcriptase assay, labelling with 3H-uridine, and membrane immunofluorescence gave no indication that retroviruses were present.
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PMID:Viruses and lymphocytes in rheumatoid arthritis. I. Studies on cultured rheumatoid lymphocytes. 53 43

Evidence for retroviral infection in general and human immunodeficiency virus (HIV) infection in particular was sought in freshly isolated peripheral blood T cells, B cells, and monocyte-macrophages from patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) and also in T cell and B cell lines established from the same source. Similar cells isolated from rheumatoid synovial membrane were also examined. The strategy used for the detection of virus was cocultivation with susceptible cell lines looking for syncytia formation, reverse transcriptase production, and nucleic acid hybridisation with HIV cDNA probes. No evidence for infection was obtained.
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PMID:A search for retrovirus infection in systemic lupus erythematosus and rheumatoid arthritis. 245 82

Immunoglobulin G (IgG) in six out of 30 patients with systemic lupus erythematosus (SLE) strongly inhibited the activity of RNA-dependent DNA polymerase (RDPase) of baboon endogenous virus, M7, while IgG obtained from scleroderma patients, rheumatoid arthritis patients and normal subjects was less reactive. Experiments with anti-human IgG and with IgG F (ab')2-bound immunoaffinity columns indicated that the inhibition of RDPase was antibody-mediated. The RDPase inhibiting activity of SLE IgG was considered not to be due to cross-reactions of anti-nuclear antibodies including anti-DNA, anti-ribonucleoprotein, anti-Sm and anti-SS.B antibodies. SLE IgG preferably inhibited the RDPase activity of baboon endogenous virus and a feline endogenous virus, RD114. These findings support the hypothesis that retrovirus(es) might be involved in SLE.
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PMID:Evidence in patients with systemic lupus erythematosus of the presence of antibodies against RNA-dependent DNA polymerase of baboon endogenous virus. 619 21

The infiltration of leucocytes into the joint of rheumatoid arthritis (RA) is believed to be mediated by chemotactic factors released by activated cells. In this study, examination was made of the gene expression and production of the chemokine superfamily in RA patients by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunoprecipitation. Cultured synovial fibroblasts were found capable of expressing and producing IL-8, GRO, monocyte chemotactic and activating factor (MCAF), macrophage inflammatory protein-1 alpha (MIP-1 alpha), MIP-1 beta and RANTES in response to IL-1 alpha. The expression of IL-8, GRO, MCAF, MIP-1 alpha, and MIP-1 beta was clearly shown to increase in freshly isolated synovial fluid mononuclear cells (SFMC) of RA patients, in contrast to peripheral blood mononuclear cells (PBMC) of RA patients and normal subjects. The gene expression of RANTES appeared to be the same for RA SFMC, RA PBMC, and normal PBMC. Thus, the over-expression of various chemokines may promote the recruitment of inflammatory cells into rheumatoid inflamed joints.
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PMID:Expression of the chemokine superfamily in rheumatoid arthritis. 752 8

We evaluated the clinical significance of the antibody to hepatitis C core protein (anti-p22) analysing 147 sera from 99 patients; 45 of them had post-transfusion non A non B (NANB) hepatitis, 28 cryptogenic non A non B hepatitis, 12 chronic hepatitis B, 7 chronic hepatitis D, 6 other forms of liver disease (4 primary biliary cirrhosis, 2 autoimmune hepatitis) and 1 rheumatoid arthritis. All sera were tested by commercial 1st and 2nd-generation ELISAs and anti-p22 single antibody ELISA. We found a highly significant correspondence between anti-p22 and commercial assays (p = 0.0001). HCV-RNA was detected by reverse transcriptase polymerase chain reaction (RT-PCR) in sera showing positive or negative concordant results and in all sera (24) that showed discordant results by anti-p22 and commercial ELISAs. HCV-RNA was found in 14 of 17 (82%) anti-p22 positive sera that were negative by commercial ELISAs, in 1 of 7 (14.3%) anti-p22 negative sera that were positive by commercial ELISAs (p = 0.001) and in all control sera from patients with positive concordant results. It was undetectable in 7 sera from patients with autoimmune diseases (negative by all ELISAs). We studied follow-up sera from 16 patients treated with interferon: 8 long-term responders (with persistently normal ALT levels for at least 24 months after discontinuation of therapy and histological remission) and 8 non-responders. Sera were also tested by a 4-antigen recombinant immunoblotting assay (RIBA II).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical significance of the antibody to the putative core protein of hepatitis C virus in patients with chronic liver disease. 769 Aug 74

Taking advantage of the reverse transcriptase-polymerase chain reaction (RT-PCR), we have analyzed T cell receptor gamma-chain mRNA of synovial fluid gamma/delta T cells from patients with rheumatoid arthritis (RA) in comparison with those of peripheral blood mononuclear cells (PBMC) from RA patients and healthy individuals. The quantitative RT-PCR method in conjunction with nucleotide sequencing revealed the frequent usage of the V gamma 3 gene segment in RA synovial fluid mononuclear cells (SFMC) (p < 0.01) which in PBMC of healthy individuals occurred rarely. PBMC of most healthy individuals expressed the V gamma 9 gene predominantly (p < 0.01) as expected. However, only half of RA patients showed elevated levels of the V gamma 9 gene expression in their PBMC. The gamma-chain mRNA containing the V gamma 3 gene in RA SFMC showed no conserved junctional sequence (complementarity-determining region 3). To investigate the nature of ligands recognized by the V gamma 3-bearing T cells, we analyzed V gamma gene usage of RA SFMC, RA PBMC, and normal PBMC stimulated with Mycobacterium tuberculosis (MT) or MT plus interleukin-2 since there is mounting evidence of high reactivity of RA SFMC to MT and mycobacterial heat-shock protein 65. However, the V gamma usage appeared to be mostly V gamma 9 in RA SFMC, RA PBMC and normal PBMC. Taken together these results suggest that an as yet unknown antigen(s) (other than MT) might select gamma/delta T cells expressing the V gamma 3 gene in RA SFMC.
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PMID:The biased V gamma gene usage in the synovial fluid of patients with rheumatoid arthritis. 818 23

In an attempt to find a potentially useful serum marker in rheumatoid arthritis (RA) which reflects underlying pathogenic mechanisms, we measured the circulating levels of matrix-degrading metalloproteinase-9 (MMP-9), also termed gelatinase B, in sera and synovial fluid (SF) from patients with RA and also quantitated the deposition and local synthesis of MMP-9 in RA synovium. Clinical samples, subjected to gelatin substrate zymography, antigenic immunoassay, and a quantitative substrate degradation assay, revealed elevated 92- and 72-kDa proenzyme forms of MMP-9 and MMP-2 in RA sera and SF compared with healthy controls. Immunostaining on fresh RA synovial specimens revealed MMP-9 within vascular walls in fibroblast-like cells and macrophages; mRNA synthesis was detected using reverse transcriptase in situ PCR. In summary, MMP-9 levels are substantially elevated in the sera and SF from patients with RA. The RA synovium is a source of this MMP-9 production, with abundant mRNA and protein observed within several different type of rheumatoid synovial cells.
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PMID:Markedly elevated serum MMP-9 (gelatinase B) levels in rheumatoid arthritis: a potentially useful laboratory marker. 862 58

Articular chondrocytes from nine arthritic patients, five infants, and Balb/c neonatal mice were analyzed for the presence of various cytokine mRNAs by a reverse transcriptase polymerase chain reaction (RT-PCR). Four cytokine mRNAs, interleukin (IL)-6, IL-8, IL-11, and macrophage colony stimulating factor (M-CSF), were detected in all human chondrocytes, regardless of source. IL-10, IL-12p35, and tumor necrosis factor alpha (TNF-alpha) transcripts were found in at least 12 of the 14 human samples. IL-13, granulocyte colony stimulating factor (G-CSF), granulocyte macrophage colony stimulating factor (GM-CSF), and TNF-beta mRNAs were found more predominantly in infant samples and in samples from patients with rheumatoid arthritis (RA) compared with samples from patients with osteoarthritis (OA). Another group of cytokine mRNAs, IL-1 (alpha, beta), IL-4, IL-5, and IL-7, were only weakly expressed in some human samples. The cytokine transcripts that were not found were IL-2, IL3, and interferon gamma (IFN-gamma). Because of the large array of cytokine transcripts detected, human chondrocyte preparations were further purified by reacting them with a monoclonal antibody specific to chondrocyte differentiation antigen and subjecting them to fluorescent-activated cell sorting. A similar array of cytokines was found between the sorted and unsorted chondrocytes, although TNF-alpha, G-CSF and GM-CSF transcripts appeared to be upregulated during the sorting process. Human chondrocytes that dedifferentiated into fibroblasts (a 40-day and a 77-day culture) no longer expressed mRNAs for IL-1, G-CSF, GM-CSF, and TNF-alpha, but all other cytokine mRNAs remained detectable. Although certain phenotypic characteristics were lost, including reactivity to chondrocyte-specific monoclonal antibodies and morphological features, chondrocytes in long-term culture still expressed cytokine mRNAs. As expected, more consistent results were obtained when seven preparations of chondrocytes from neonatal Balb/c mice were examined using available cytokine primers. They contained IL-1, IL-5, IL-6, IL-7, IL-12, GM-CSF, M-CSF, transforming growth factor beta (TGF-beta), TNF-alpha, and TNF-beta mRNAs but lacked IL-2, IL-3, IL-4, IL-10, and IFN-gamma mRNAs. Future experiments to define conditions by which these cytokine protein products are expressed are needed to help assess their roles in chondrocyte biology and in disease states.
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PMID:Cytokine mRNA repertoire of articular chondrocytes from arthritic patients, infants, and neonatal mice. 885 28


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