Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003873 (rheumatoid arthritis)
 53,068 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have determined the distribution of T gamma delta cells in the peripheral blood of 44 patients with rheumatoid arthritis and in 36 healthy controls. In addition, paired blood and synovial fluid samples were obtained from seven patients with RA. The monoclonal antibodies A13, BB3 and Ti gamma A, which are specific for the V delta 1, V delta 2 and V gamma 9 gene products respectively, were used to define T gamma delta subsets. T gamma delta + cells expressed as a percentage of CD3+ lymphocytes were reduced in RA peripheral blood compared with the control group (3.9% +/- 0.5 versus 5.7% +/- 0.7; P less than 0.0001). There was a reduction in the V gamma 9/V delta 2+ subset (from 5.6% +/- 1.2 to 1.7% +/- 0.4) leading to a change in the mean ratio of V delta 2/V delta 1+ cells from 4.3 in normal subjects to 1.1 (P less than 0.002). No statistical difference was observed in T gamma delta cell numbers in synovial fluid compared with the paired blood samples (4.0% +/- 1.1 in blood and 4.4% +/- 1.4 in synovial fluid). Also the distribution of V delta 2+ and V delta 1+ cells was similar in the two compartments and a similar alteration in subset distribution was found in blood and synovial fluid. These findings do not indicate a selective accumulation of a specific T gamma delta subset in RA synovial effusions.
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PMID:T gamma delta cells and their subsets in blood and synovial fluid from patients with rheumatoid arthritis. 138 49

The distribution of T-lymphocytes expressing CD3 and T-cell receptor gamma-delta (T gamma/delta) has been examined by immunocytochemistry in the synovial membrane of eight patients with inflammatory arthritis (six rheumatoid arthritis, two spondyloarthritis) and eight with non-inflammatory arthritis (four osteoarthritis, four post-traumatic arthritis). T gamma/delta cells were present in eight out of eight inflammatory arthritis synovial membranes, but in only one out of eight non-inflammatory membranes (P less than 0.005). The mean T gamma/delta percentage (of total T-cells) in inflammatory arthritis was 14% (range 7-25%). T gamma/delta cells were found mainly in the transitional area of the synovial membrane with a scattered distribution as single cells or couplets. No relation was found between the presence and percentage of T gamma/delta cells and disease duration or steroid treatment.
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PMID:T-cell receptor gamma-delta positive lymphocytes in synovial membrane. 153 Sep 10

Taking advantage of the polymerase chain reaction we have studied the usage of variable delta-(V delta) region genes in freshly isolated synovial fluid T cells from patients with rheumatoid synovitis. Amplified mRNA from one patient with rheumatoid arthritis (RA) was cloned into an SmaI-cleaved pUC19 vector and colonies were screened with probes for three of the known human variable delta-gene families (V delta 1, V delta 2, V delta 3). Of 10 clones, seven used V delta 1, two V delta 2 and one V delta 3. This pattern of distribution is different from that of normal peripheral blood, where approximately 60% of T gamma delta cells are reported to use the V delta 2 gene. Furthermore, Northern blot hybridization analyses of mononuclear cells from two additional synovial fluids derived from another patient with RA and one with juvenile rheumatoid arthritis (JRA) also showed significant hybridization only with V delta 1. In summary, these preliminary results suggest a usage of V delta gene families in T gamma delta lymphocytes in synovial fluid of rheumatoid patients different to that found in normal peripheral blood.
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PMID:The V delta gene usage by freshly isolated T lymphocytes from synovial fluids in rheumatoid synovitis: a preliminary report. 169 53

T cell receptor (TCR) gamma/delta bearing lymphocytes in peripheral blood and synovial fluid from rheumatoid arthritis (RA) and seronegative spondyloarthritides (SSA) were evaluated by means of double label immunofluorescence and cytofluorographic analysis. Three monoclonal antibodies (MAb) were used. TCR delta-1 against a common delta chain epitope, BB3 directed against the T cell subset whose TCR is encoded by the V delta 2 gene, and A13 directed against the V delta 1 subset. Peripheral blood T gamma delta cells were significantly reduced compared to normal control blood in RA patients who had joint effusion but not in other RA patients. The decrease of T gamma delta in the RA PB was mainly confined to the A13+ subset. In RA synovial fluid (RA SF) T gamma delta cells were significantly increased compared to paired but not normal peripheral blood, the most significant being the increase of A13+ cells. In contrast, in patients with SSA, no change in T gamma delta cells was observed on PB or SF. These data suggest that in RA, but not SSA, T gamma delta cells migrate from PB to inflamed synovium and thus may be involved in the pathogenesis of RA.
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PMID:Gamma/delta T cells and their subpopulations in blood and synovial fluid from rheumatoid arthritis and spondyloarthritis. 182 66

Using immunohistology and monoclonal antibodies directed to the T-cell receptor (TCR) chains, we have analysed the distribution of TCR-bearing lymphocytes within the membrane of rheumatoid arthritis (RA) patients. Alkaline phosphatase staining for TCR alpha beta-bearing lymphocytes showed a distribution paralleling that of the total T cells. Staining for the TCR gamma delta chains revealed a moderate and rather homogeneous distribution of T gamma delta lymphocytes within the RA synovium. As evidenced by simultaneous staining for alpha beta and gamma delta receptors, the relative count of T gamma delta to alpha beta-expressing cells is close to the peripheral count (e.g.5%), and lower than that previously observed in the synovial fluid. Interestingly, the peripheral type V gamma 9-J gamma P rearrangement using the T gamma delta cell subset was relatively decreased in the synovial membrane, as compared to synovial fluid and peripheral blood, suggesting that the T gamma delta distribution in the rheumatoid synovium resembles a thymic-like situation.
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PMID:Distribution of T-cell receptor-bearing lymphocytes in the synovial membrane from patients with rheumatoid arthritis. 208 92

We have examined the frequencies of T gamma delta cells in blood, synovial fluids, and synovial membranes of patients with rheumatoid arthritis (RA) and in blood from age-matched controls. Immunocytochemical and immunohistochemical techniques were used with monoclonal antibodies BB3 and A13 to define a major and minor blood subset of T gamma delta cells respectively. Together, these antibodies identify the majority (if not all) of the peripheral blood T gamma delta cells. Significantly lower levels of T gamma delta cells were found in the blood of RA patients compared with controls, whilst higher but not significant numbers were found in the synovial fluids of paired samples. Scattered T gamma delta cells were found only in some synovial membranes with a distribution similar to the T alpha beta cells. Analysis of the two different T gamma delta-cell subsets indicated a ratio of BB3 to A13 of about 5:1 in control and RA blood. However, this ratio was less than 1:1 in the RA synovial fluids and membranes. The migratory nature of the A13+ cells could account for their predominance in these sites. The possible pathological significance of these cells in the rheumatoid synovial fluid and synovial membranes is discussed.
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PMID:T gamma delta cells and their subsets in blood and synovial tissue from rheumatoid arthritis patients. 214 40

Using the anti-TcR gamma/delta-1 monoclonal antibody and flow cytometry, we examined the number of T gamma delta cells in paired samples of peripheral blood and synovial fluid or tissue from 24 children with juvenile rheumatoid arthritis (JRA), five adult patients with JRA, and 14 patients with rheumatoid arthritis (RA). No significant difference was found in the synovial compartment T gamma delta values compared with the blood in JRA, adult JRA, or RA patients. Nor was any significant difference found in the peripheral blood or synovial compartment T gamma delta values in any of the three patient groups compared with the peripheral blood of normal controls. However, seven of the children with JRA had very high T gamma delta values in the synovial compartment while none of the normal children had high T gamma delta values in the blood (P = 0.02, Fisher's exact test). This may indicate a possible separate JRA patient group with high T gamma delta levels in the synovial compartment. In six JRA patients further analysed for T gamma delta subpopulations, a significant predominance of V delta 1+ cells was found in the synovial compartment compared with the corresponding peripheral blood samples (P less than 0.05, Wilcoxon's signed test) and with peripheral blood of child controls (P less than 0.05, Mann-Whitney U test). In these six patients, the T gamma delta-cell expression of the very early activation antigen CD69 were significantly higher (P less than 0.05, Wilcoxon's signed test) in the synovial compartment compared with the peripheral blood. Synovial T gamma delta cells expressing HLA-DR and interleukin 2 receptors could also be detected, in contrast to the peripheral blood in which no T gamma delta cells expressing these antigens could be found. These data suggest that the synovial T gamma delta cells had been activated in vivo.
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PMID:T gamma delta cells in juvenile rheumatoid arthritis and rheumatoid arthritis. In the juvenile rheumatoid arthritis synovium the T gamma delta cells express activation antigens and are predominantly V delta 1+, and a significant proportion of these patients have elevated percentages of T gamma delta cells. 214 43

We assessed the immunoglobulin secretory capacity of circulating B lymphocytes in 9 patients with classical rheumatoid arthritis (RA) before and after treatment with D-penicillamine. Peripheral blood lymphocytes (PBL) from patients with RA spontaneously synthesized more IgG and IgA than normals. The secretory rate of rheumatoid PBL could not be induced by the polyclonal activator, pokeweed mitogen (PWM). The presence of D-penicillamine in cultures significantly suppressed PWM stimulated immunoglobulin synthesis of control PBL but did not inhibit synthesis of mitogen stimulated RA PBL. After D-penicillamine therapy for 3 months immunoglobulin synthesis by PBL from patients with RA was reduced with or without PWM. The T mu:T gamma ratio was also decreased after therapy. These results support the hypothesis that D-penicillamine selectively impairs helper T cells in vivo, preventing the T dependent expansion and activation of B cells characteristic of RA.
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PMID:D-penicillamine induced suppression of B cell function: in vivo effect of D-penicillamine. 387 66

Monoclonal antibodies with specificities for various human T-cell antigens were used in direct immunofluorescence to quantify the proportions of T lymphocytes with suppressor/cytotoxic-cell markers and with helper/inducer-cell markers and of T lymphocytes with HLA-DR antigens. Normal percentages of lymphocytes with suppressor/cytotoxic-cell markers were detected in the peripheral blood synovial fluid and synovial tissue lymphocytes from patients with juvenile rheumatoid arthritis (JRA) and rheumatoid arthritis (RA), respectively. Normal percentages of T lymphocytes with helper/inducer-cell markers were seen in the peripheral blood of RA and JRA patients and in the synovial tissues of RA patients. Slightly decreased percentages of cells with the helper/inducer-cell marker were detected in the synovial fluids of JRA patients. The proportions of HLA-DR-positive T lymphocytes were highly increased in the synovial fluid and synovial tissue, whereas the numbers of these cells in the peripheral blood were normal. No significant differences in T gamma cells were detected between peripheral blood, synovial fluid and synovial tissue of JRA patients or between peripheral blood and synovial tissue of RA patients.
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PMID:Detection of T-lymphocyte subpopulation in the peripheral blood and the synovium of patients with rheumatoid arthritis and juvenile rheumatoid arthritis using monoclonal antibodies. 621 26

The immunopathogenesis of rheumatoid synovitis (RS) is assumed to be as follows: antigen X interacts with the organism of subjects genetically predisposed to rheumatoid arthritis (RA) as a result of which the immune response regulation is disturbed ("immunological discomfort") leading to changes in proliferation and differentiation of immunocompetent cells immunologically manifested by disturbed ratios of lymphocyte subpopulations and morphologically by immune inflammation of synovial membranes, i.e. RS. Immune inflammation in RS is a systemic, chronic, persisting, recurrent, self-sustained process based on profound changes in qualitative and quantitative aspects of immunological homoeostasis. The results of the authors' own studies indicate that in the inflammation field (eluates of synovial membrane and synovial fluid) rearrangement of lymphocyte subpopulations is more marked than in the peripheral blood of patients with RA. The quantitative deficiency in eluates of synovial membrane and peripheral blood of T gamma-lymphocytes having the suppressive-cytotoxic function confirms the important role of immunoregulation disturbance in the pathogenesis of RA.
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PMID:[Rheumatoid synovitis (problems of immunomorphology and immunopathogenesis)]. 628 82


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