SEARCH · Search PubMed

Results for “SYNOVIAL FLUID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,477 records · Page 82Linked to original sources

PubMed1997

IgG2b inducing factor from rheumatoid arthritis synovial fluid activates antibody production in highly purified mouse B lymphocytes.

Rheumatoid arthritis synovial fluid (RA-SF) contains a factor that induces IgG2b antibody production in LPS-stimulated murine B cells and therefore is called IgG2b inducing factor (IgG2bIF). When LPS, together with crude RA-SF or semi-purified IgG2bIF, was added to highly purified LPS-stimulated B cells, the number of IgG2b-producing cells was substantially enhanced. This shows that IgG2bIF acts directly on activated B cells, presumably by binding to a receptor expressed on LPS-activated B cells. In vivo LPS-activated B blasts were not able to respond to RA-SF unless LPS was present in vitro, showing that LPS is needed to maintain cell viability and responsiveness to the IgG2bIF. To elucidate the mechanism for the IgG2bIF effect on highly purified B cells, the IgG2b response of LPS-stimulated, Bruton's tyrosine kinase-defective, xidB blasts was studied. Purified B blasts from the btk-defective CBA/N mouse strain were sensitive to IgG2bIF. These findings show that IgG2bIF acts directly on B cells and activates cells through a btk-independent pathway.

Animals↗

PubMed1999

Matrix metalloproteinases, tissue inhibitors of metalloproteinases, and glycosaminoglycans in synovial fluid from patients with rheumatoid arthritis.

OBJECTIVE: To investigate the correlation between synovial fluid (SF) concentrations of metalloproteinase (MMP) -2, -3, and -9, tissue inhibitors of metalloproteinases (TIMP)-1 and -2, chondroitin 4-, 6-sulfate (deltadi-C4S, deltadi-C6S), hyaluronic acid (deltadi-HA), antigenic keratan sulfate (KS), and radiologic grade in patients with rheumatoid arthritis (RA) and to assess the clinical value of these factors as disease markers. METHODS: Enzyme linked immunoassays and high performance liquid chromatography were used. SF samples were collected from 52 patients with RA. Radiographic (Larsen grade) and clinical evaluations were also done. RESULTS: There was no significant correlation between the concentrations of MMP, TIMP, and deltadi-C4S, deltadi-C6S, deltadi-HA, and antigenic KS. No significant correlations were found between the radiologic grade and the concentrations of MMP or TIMP in SF. There was a significant increase in the concentration of antigenic KS and deltadi-C6S/deltadi-C4S ratio in SF from patients with Larsen grade 2 compared to grade 5. A significant correlation between deltadi-C6S and antigenic KS concentrations in SF was observed. CONCLUSION: Although there were large variances between the samples in this study, proteoglycan metabolism in the cartilage matrix of the patients with RA might have been increased in the early phases of tissue destruction and decreased in advanced stages because of scanty cartilage tissue. The concentrations of MMP-2, -3, -9 and TIMP-1, -2 in SF did not seem to be influenced by the amount of residual cartilage.

Aged↗

PubMed1988

Phospholipase A2 activity associated with synovial fluid cells.

High activity of phospholipase A2 (PLA2) has been detected in synovial fluids (SF) in inflammatory arthritides. Since the source(s) of SF PLA2 has not been identified, we tested PLA2 content in SF cells obtained from 11 SF. Cell sonicates were prepared at 5 X 10(6) cells/ml. In the supernatants of the sonicated SF cells (n = 11), PLA2 activity ranged from 38-755 U/ml, mean 368 +/- 243 (SD) U/ml, compared to 5-64 U/ml, mean 31 +/- 15 (SD) U/ml in sonicates of normal peripheral blood PMN (n = 5) (p less than 0.0001). Spontaneous release of PLA2 from unstimulated SF cells ranged from 26-365 U/ml, mean 131 +/- 144 (SD) U/ml (n = 5), whereas spontaneous release from peripheral blood PMN was negligible. Neither 10(-8) M FMLP nor 5 X 10(-6) M dexamethasone altered extracellular PLA2 release. To assess whether PLA2 adsorbs passively to cell membranes through hydrophobic interaction, normal peripheral PMN were incubated in crude SF (n = 7) with PLA2 ranging from 4,000-24,300 U/ml, or with purified human SF PLA2 or Naja naja PLA2. We found that soluble PLA2 adsorbed to PMN membranes in a concentration dependent fashion. PLA2 activity in sonicates of PMN incubated in crude SF ranged from 185-358 U/ml compared to controls of 21-64 U/ml. Sonicates of PMN incubated with purified human SF PLA2 (5,000-30,000 U/ml) showed progressive concentration dependent increase in PLA2 from 7 +/- 4 to 212 +/- 11 (SD) U/ml (p less than 0.001). PMN incubated with Naja naja PLA2 also showed marked increase in the content of PLA2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adsorption↗

PubMed1989

Occurrence of interleukin-1 in human synovial fluid: detection by RIA, bioassay and presence of bioassay-inhibiting factors.

Synovial fluid (SF) from patients with osteoarthritis (OA), rheumatoid arthritis (RA), and various other arthridites was analyzed to assess the prevalence of interleukin-1 (IL-1) using both radioimmunoassay competitive inhibition specific for the beta form of IL-1 and the D10.G4.1 cell line bioassay which measures both alpha and beta forms of IL-1. Using radioimmunoassay competitive inhibition, IL-1 beta was found in 45% and 60% of individual samples from patients with OA and RA respectively. When RA and OA SF were examined in sequentially obtained samples, IL-1 beta occurred in one or more samples from 8 of 10 patients studied, suggesting the probability that it can be produced at some time in SF by all patients with these conditions. No correlation between SF leukocyte counts and the occurrence of IL-1 beta was noted and no effect of antiinflammatory drug treatment on the prevalence of IL-1 beta was found. When tested for the presence of IL-1 by the D10.G4-1 cell line, 66% and 50% of RA and OA patients respectively were found to contain IL-1. These were not in total concordance with results obtained by RIA. Of all SF tested, seven were negative by RIA but positive by D10.G4.1 and these are considered to contain IL-1 alpha. Seven samples which were RIA positive and D10.G4.1 negative were tested for their ability to inhibit IL-1 responses in the bioassay. Five of these contained inhibitor and one markedly enhanced the proliferative response of D10.G4.1 to a known amount of IL-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Arthritis, Rheumatoid↗

PubMed1992

Measurement of elastase and cysteine proteinases in synovial fluid of patients with rheumatoid arthritis, sero-negative spondylarthropathies, and osteoarthritis.

Synovial fluid samples were collected from 45 patients with rheumatoid arthritis, spondylarthropathy, or osteoarthritis, to study their content of elastase (EC 3.4.21.37) and of cysteine proteinases (EC 3.4.22.1, 3.4.22.15). We measured both elastase complexed with alpha 1-proteinase inhibitor and elastase activity toward the substrate L-pyroglutamyl-L-prolyl-L-valine-p-nitroanilide. Cysteine proteinase activities were measured with the substrates N-benzyloxycarbonyl-L-phenylalanyl-L-arginine-7-amido-4-methylcoumarin (Z-Phe-Arg-AMC) and Z-Arg-Arg-AMC and the inhibitor E-64 [L-trans-epoxysuccinyl-leucyl-amido-(4-guanidino)-butane]. In all these enzyme assays, higher median values were obtained in inflammatory arthropathies than in osteoarthritis. The concentration of the elastase-alpha 1-proteinase inhibitor complex and of elastase and cysteine proteinase activities were statistically higher in patients with rheumatoid arthritis than in patients with osteoarthritis. The difference in results between patients with spondylarthropathy and patients with osteoarthritis was statistically significant only for the elastase-alpha 1-proteinase inhibitor complex. The median values of the complex and of both enzyme activities were higher in patients with rheumatoid arthritis than in patients with spondylarthropathy; however, the difference was statistically significant only for the cysteine proteinase activity measured with Z-Arg-Arg-AMC substrate. These results suggest that both elastase and cysteine proteinases, which are increased in patients with inflammatory arthritis, are involved in cartilage degradation in these arthropathies.

Adolescent↗

PubMed2000

Influence of development and joint pathology on stromelysin enzyme activity in equine synovial fluid.

OBJECTIVE: To investigate the role of stromelysin (MMP-3) activity in synovial fluid (SF) at different stages of development and in common joint disorders in the horse. METHODS: Stromelysin activity was determined with a fluorogenic enzyme activity assay in SF of normal joints of fetal, juvenile and adult horses, and in SF of horses suffering from the developmental orthopaedic disease osteochondrosis (OC) or osteoarthritis (OA). Additionally, MMP-3 activity was expressed as a ratio of previously reported general MMP activity in the same SF samples. RESULTS: The levels of active stromelysin were 30-fold to 80-fold higher in SF from fetal horses than in SF from juvenile and mature animals (p<0.001). Juvenile horses (5 and 11 months of age) showed a twofold to threefold higher stromelysin activity than adult horses ( p<0.05). In OC joints, stromelysin activity was not significantly different from the activity in normal, age matched, control joints. In OA joints the activity was about four times higher than in normal joints (p<0.001). The ratio MMP-3 activity/general MMP activity did not change with age in normal, healthy joints. This ratio was more then twofold increased in OA joints compared with normal joints, indicating selective upregulation of gene expression or activation of proMMP-3, or both, in OA pathology. CONCLUSIONS: The significantly higher stromelysin activity in young individuals parallels the higher metabolic activity occurring at rapid growth and differentiation at early age. In OC, MMP-3 mediated matrix degradation appears to be not different from normal joints. The increased stromelysin activity in OA joints is in agreement with pathological matrix degradation. In these joints MMP-3 activity is selectively increased compared with normal joints.

Aging↗

PubMed1984

Demonstration of fibronectin associated with platelets in synovial fluid from patients with rheumatoid arthritis.

Paired samples of peripheral blood and synovial fluid (SF) aspirated from inflamed knee joints from 15 adult patients with classical rheumatoid arthritis, as well as peripheral blood obtained from 15 healthy subjects, were anticoagulated with ACD. Peripheral blood platelets were separated from other plasma constituents by gel filtration of platelet-rich plasma on Sepharose 2B. When using this technique on SF, it was found that platelets could be isolated from other SF constituents, and that each of the SF's gave a high yield of eluted platelets. Direct immunofluorescent staining for human fibronectin was performed with isolated and suspended platelets obtained from the three different sources. Aliquots of both intact and permeabilized platelets were stained. Intact peripheral platelets from all patients and normal subjects revealed a weakly positive staining, whereas the staining of intact SF platelets from all patients was clear and bright. The fluorescence of intact cells was surface-located and speckled. For permeabilized platelets, the staining had a punctate intracellular pattern, with a varying number of discrete and bright fluorescent foci per cell. Counting of the foci in each platelet specimen revealed that this number, which was also found in peripheral platelets from all patients and normal subjects, was distinctly greater than the number of foci in all the SF platelet specimens. No relationship was found between the various staining results and medical treatment or Waaler-Rose serology of the patients. The findings indicate that the SF platelets had large amounts of surface-bound and small amounts of intracellular fibronectin, whereas the converse was found in the case of peripheral platelets from the patients and normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Differential sensitivity to transforming growth factor (TGF)-beta of CBA and of CBA/N B cells demonstrates that the IgG2b inducing factor in synovial fluid from rheumatoid arthritis patients is not identical to TGF-beta.

Synovial fluid from patients with rheumatoid arthritis (RA-SF) contains in vivo produced cytokines and inflammatory mediators, including a factor that induces IgG2b production of lipopolysaccharide (LPS) preactivated murine B lymphocytes. In order to determine the mechanism by which RA-SF acts on LPS activated mouse B cells, CBA/N mice were used as an experimental model. The X-linked immunodeficiency of these mice is caused by a point mutation in the Bruton's tyrosine kinase (btk) gene. We have earlier shown that RA-SF can reconstitute the CBA/N B cell deficiency in vitro and in vivo, with regard to IgG2b production after LPS stimulation. Since transforming growth factor (TGF)-beta has been suggested to be a switch factor for IgG2b, we aimed at investigating the role of TGF-beta in our experimental system. We found that TGF-beta could not mimic the effect of RA-SF on CBA spleen cells. A small increase of IgG2b secretion was observed with spleen cells from normal CBA mice, whereas Ig secretion of all isotypes was suppressed in CBA/N spleen cells treated with TGF-beta at any concentration. Neutralizing antibodies against TGF-beta suppressed the response of CBA B cells, whereas the response by CBA/N B cells was enhanced by the same antibody preparation. Here we also show that the abnormal B cell responsiveness to TGF-beta, typical of CBA/N, co-segregates with the btk mutation in male (CBA x CBA/N)F2 spleen cells. This was determined by allele specific PCR recognizing the identified base substitutions of the btk gene, typical of the two strains. We propose that RA-SF contains a factor, separate from TGF-beta, that is involved in the differentiation of IgG2b expressing cells.

Agammaglobulinaemia Tyrosine Kinase↗

PubMed1988

Neoantigenic group on Fc fragments in rheumatoid arthritis synovial fluids.

Expression of neoantigens during denaturation of IgG by oxygen radicals or proteolysis was assumed to be a possible mechanism for stimulation of rheumatoid factor (RF) formation and/or granulocyte dependent inflammative joint destruction. The so-called human leukocyte elastase (HLE) regularly released by stimulated neutrophils f.e. into the RA synovial fluid is known to split IgG in vitro into papain like fragments and low molecular weight peptides. The n-terminal site of the HLE related Fc is bearing a neoantigenic group which is located near the hinge region but not expressed by the native IgG. The neoantigen itself is represented by the low molecular weight peptides produced by prolonged HLE-IgG proteolysis. Detection of HLE generated Fc in synovial fluids was performed by radioimmunoassay specific for the neoantigen. Patients were divided into the three groups; I RA (n = 23), II inflammative joint effusions except RA (n = 23), III osteoarthritis and trauma (n = 19). The biological effect of the neoantigen on to granulocyte oxidative metabolism was tested by Cytochrome C reduction and chemiluminescence. Neoantigen bearing Fc could be detected in 15 of 23 cases of group I, in group II in 11 of 23 cases and only in 7 of 19 cases in group III. The median concentrations were 0.62 micrograms in group I and zero in II and III. The HLE derived Fc were able to inhibit the oxidative metabolism of activated granulocytes in vitro. The O2- production of stimulated granulocytes was depressed dose dependent by the neoantigen. The neoantigenic group itself does not react with RF as proved by nephelometric titration of HLE derived Fc, neoantigenic peptide and native IgG against a RF standard.

Antigens↗

PubMed2006

Optimization of an enzymatic method for the determination of lysosomal N-acetyl-beta-D-hexosaminidase and beta-glucuronidase in synovial fluid.

BACKGROUND: Our goal was to develop a suitably sensitive assay for N-acetyl-beta-D-hexosaminidase (HEX) and beta-glucuronidase to allow their use as markers of joint diseases. METHODS: We optimized a spectrophotometric method for the determination of lysosomally derived HEX and beta-glucuronidase in synovial fluid on a microplate reader to improve its utility. HEX and beta-glucuronidase act on the 4-nitrophenyl derivatives N-acetyl-beta-glucosamine and beta-D-glucuronide, respectively, to produce 4-nitrophenol, which can be measured at 405 nm on a microplate reader. RESULTS: Maximum enzyme activity was observed at pH 4.7 in a citrate-phosphate buffer for HEX and at pH 4.5 in an acetate buffer for beta-glucuronidase. A 10-microL sample with 30 microL of substrate solution and 40 microL of appropriate buffer produced measurable amounts of 4-nitrophenol after incubation for 60 min at 37 degrees Celsius. Reactions were terminated by the addition of 200 microL of 200 mM borate buffer (pH 9.8). CONCLUSIONS: The assay is sufficiently sensitive for small volumes of synovial fluid, and is useful for the clinical diagnosis of joint diseases.

Aged↗

PubMed2003

Electrophoretic characterization of species of fibronectin bearing sequences from the N-terminal heparin-binding domain in synovial fluid samples from patients with osteoarthritis and rheumatoid arthritis.

Fragments of fibronectin (FN) corresponding to the N-terminal heparin-binding domain have been observed to promote catabolic chondrocytic gene expression and chondrolysis. We therefore characterized FN species that include sequences from this domain in samples of arthritic synovial fluid using one-and two-dimensional (1D and 2D) Western blot analysis. We detected similar assortments of species, ranging from ~47 to greater than 200 kDa, in samples obtained from patients with osteoarthritis (n = 9) versus rheumatoid arthritis (n = 10). One of the predominant forms, with an apparent molecular weight of ~170 kDa, typically resolved in 2D electrophoresis into a cluster of subspecies. These exhibited reduced binding to gelatin in comparison with a more prevalent species of ~200+ kDa and were also recognized by a monoclonal antibody to the central cell-binding domain (CBD). When considered together with our previous analyses of synovial fluid FN species containing the alternatively spliced EIIIA segment, these observations indicate that the ~170-kDa species includes sequences from four FN domains that have previously, in isolation, been observed to promote catabolic responses by chondrocytes in vitro: the N-terminal heparin-binding domain, the gelatin-binding domain, the central CBD, and the EIIIA segment. The ~170-kDa N-terminal species of FN may therefore be both a participant in joint destructive processes and a biomarker with which to gauge activity of the arthritic process.

Antibodies, Monoclonal↗

PubMed1987

[Prostaglandin E2 liberation in the synovial fluid induced by organo-iodinated contrast media. Interrelations with the genesis of post-arthrographic pain].

RCM have been observed to cause--during arthrography--the appearance of a slow onset painful symptomatology with the clinical characteristics of a slight and transient acute arthritis. These substances are supposed to set in a production of humoral mediators of inflammation with algogenic action--PGE2 in particular. During arthrography of the knee the release of synovial fluid PGE2 after RCM introduction was studied. Two RCM were compared: meglumine iothalamate and iopamidol. Twenty patients underwent arthrography of the knee: synovial fluid PGE2 concentration was measured both before and 15' after RCM introduction with 125I-RIA method. Results show a significant increase in PGE2 concentration after both iothalamate (p less than 0.0001) and iopamidol (p less than 0.01) --especially in iothalamate--treated patients (p less than 0.01). A physiopathologic mechanism about post-arthrographic pain and, more generally, about RCM toxicity is thus hypothesized.

Arthrography↗

PubMed1994

Synovial fluid as a matrix of selection in the detection of beta-adrenergic agonist drugs in carcases and fresh meat.

Previous papers have supported the hypothesis that beta-agonist drugs could accumulate in those tissues with a high content of mucopolysaccharides. Based on our preliminary findings, between October and December 1993 we randomly sampled 534 samples of synovial fluids drawn from the knee joint of fresh carcasses. After a preliminary extraction able to break down the water domains of mucopolysaccharides and the interactions between the matrix and the drugs, samples were concentrated on diatomaceous earth and then screened on two different ELISA plates. We confirmed the structure of suspected fluids by GC-MS (HFBA derivatization), according to EC criteria. Of the 57 samples screened as positive (10.6% of the total), 51 (9.5%) were fully confirmed, while for six it was not possible to identify the drug. The results suggest that the analysis of synovial fluids is an adequate tool to monitor the misuse of beta-adrenergic drugs in animal production, especially when target organs such as liver and kidney are not available for sampling.

Adrenergic Agonists↗

PubMed1994

ELISA for the core protein of the cartilage large aggregating proteoglycan, aggrecan: comparison with the concentrations of immunogenic keratan sulphate in synovial fluid, serum and urine.

Immunological assays for fragments of the cartilage large aggregating proteoglycan, aggrecan, have been widely used to monitor cartilage turnover. These assays have commonly employed the monoclonal keratan sulphate antibody, 5D4. Keratan sulphate, however, is present in many tissues and 5D4 affinity is critically dependent on antigen structure. We have therefore raised and characterized a monoclonal antibody (1-F21) that reacts with the core protein of aggrecan without interference from the glycosaminoglycan side chains and, using this antibody, we have optimized a sensitive, competitive ELISA. The within-assay and between-assay coefficients of variation were 4.9-8.9% and 11.1-13.0%, respectively. The mean concentrations of core protein in synovial fluid, serum and urine were 76.4 micrograms/ml, 104.0 ng/ml and 81.0 ng/ml, respectively. In synovial fluids the concentrations were closely correlated with the concentrations of keratan sulphate as determined by 5D4 (r = 0.94), whereas in serum and urine there was no obvious correlation between the determinations. These findings show that measurement of both core protein and keratan sulphate results in a more precise description of aggrecan turnover.

Aggrecans↗

PubMedDate not supplied

Treatment of juvenile idiopathic arthritis with intra-articular triamcinolone hexacetonide: evaluation of clinical effectiveness correlated with circulating ANA and T gamma/delta + and B CD5+ lymphocyte populations of synovial fluid.

OBJECTIVE: The aims of the study were to assess the effect of intra-articular treatment with triamcinolone hexacetonide (TH) in juvenile idiopathic arthritis (JIA) and to investigate whether treatment response correlates with the presence of antinuclear antibodies (ANA) in the serum and/or B CD5+ and T gamma/delta + lymphocytes in the synovial fluid. METHODS: A total of 37 patients (81% females, 56% ANA+) with oligoarticular JIA involving knees were treated with intra-articular injections of TH after failing to respond to NSAIDs for two months. Eighteen patients were treated within 6 months of onset, 19 were treated more than 6 months after onset. RESULT: Mean duration of remission was 13.9 months. Twelve patients (7 ANA+) had stable remission after a single injection; 13 patients (3 ANA+) experienced more than 6 months' remission but subsequently had a relapse; 12 patients (11 ANA+) had a relapse within six months of injection. Of 20 patients treated within 6 months of onset, 17 had stable remission whereas only 8 out of 17 who were treated during relapse attained stable remission (p = 0.03). The mean percentage of T gamma/delta + and of B CD5+ lymphocytes in synovial fluid was the same as in peripheral blood of normal subjects. CONCLUSION: Our data indicate that local treatment with slow-release steroids is very effective in oligoarticular JIA. Prolonged remission was less likely in the presence of ANA positivity, probably because the disease is immunologically more active. Finally, our data suggest that the earlier the treatment, the easier it is to obtain a protracted, and possibly permanent, response.

Anti-Inflammatory Agents↗

PubMed1984

[Molecular biology studies of synovial fluid cells of patients with chronic polyarthritis after intra-articular prednisolone medication].

In the course of molecular biological research on patients with classical rheumatoid arthritis (according to ARA criteria), an investigation was carried out on the influence of different doses of prednisolone on semiconservative DNA synthesis, the sedimentation of nucleoids before and after gamma-irradiation and protein synthesis in synovial fluid cells. A significant dose-dependent suppression of semiconservative DNA synthesis was demonstrated with 5, 10 and 25 mg prednisolone. Granulocytes and cell detritus were removed by Ficoll urografin separation. In the presence of high saline concentrations and non ionic detergents nucleoids were extracted from synovial cells. These contained, besides nuclear proteins, almost the complete nuclear RNA and DNA in a superhelical structure. After ultracentrifugation, the nucleoid sedimentation profiles were determined by saccharose gradients. The individual sedimentation profiles were determined and statistically evaluated before and after irradiation causing strand breaks by Co60 at a dose of 1 Gy. No difference in nucleoid sedimentation was seen at a dosage of 5 mg of prednisolone, but after administration of 10, 25 and 40 mg a decrease in sedimentation velocity was observed and this effect might be explained by the DNA destabilizing effect of a steroid receptor complex followed by DNA strand breaks which had migrated into the nucleus. In vitro, no significant inhibition of supercoiled DNA repair was found after gamma-irradiation when prednisolone was administered. This is an argument against a damaging influence of prednisolone on the DNA repair of the genetic material of synovial fluid cells, which are predominantly lymphocytes. For the investigation of protein synthesis, 3H-labelled L-aminoacids were incorporated into the cells, and the activity measured after repeated washings. Following the administration of the lower prednisolone doses (5 and 10 mg) the incorporation of 3H-labelled L-aminoacids increases, whereas a significant inhibition of protein synthesis is found with doses of 25 mg or more. The possible clinical relevance of this phenomenon is discussed.

Amino Acids↗

PubMed1985

Effect of drug therapy on circulating and synovial fluid Ig-secreting cells in rheumatoid arthritis.

A common immunological abnormality in rheumatoid arthritis (RA) is an increased spontaneous polyclonal B cell activation. In order to study the influence of drug therapy in RA on the functional activity of B cells we enumerated spontaneous plaque-forming cells (PFC) in peripheral blood lymphocytes (PBL) and synovial fluid lymphocytes (SFL) by a reverse haemolytic plaque assay. Spontaneous IgG-, IgM-, and IgA-PFC in PBL of 26 patients with classical erosive RA receiving either gold salts or D-penicillamine were similar to those observed in 20 healthy controls. In contrast, significantly higher numbers of IgG- and IgA-PFC, but not IgM-PFC, were found in PBL of nine patients with classical erosive RA receiving non-steroidal anti-inflammatory drugs (NSAID) alone. Furthermore, spontaneous PFC in SFL from 16 consecutive patients with RA receiving second-line drugs, as well as 17 patients with other forms of arthritis (non-RA) were generally low and significantly less than those observed in 20 RA patients on NSAID alone. Moreover, a wide individual variation in PFC, especially in relation to the IgG class, was recorded in the synovial lymphocytes. These studies imply that treatment with second-line drugs is associated with normalisation of B cell activity in RA patients, and that the effect can be detected at the cellular level both in blood and synovial fluid.

Adult↗

PubMed1996

Successful induction of severe destructive arthritis by the transfer of in vitro-activated synovial fluid T cells from patients with rheumatoid arthritis (RA) in severe combined immunodeficient (SCID) mice.

In order to investigate the role of pathogenic T cells in RA, the establishment of an RA model using patients' T cells is thought to be essential. In this study, multiple and severe destructive arthritis was established by transferring in vitro-stimulated synovial fluid T (SFT) cells from patients with RA through simultaneous injection into knee joint and peritoneal cavity of SCID mice without causing xenogeneic graft-versus-host disease (GVHD). Neither the transfer of unstimulated SFT cells nor sole i.p. injection was sufficient to induce severe arthritis. Interestingly, in contrast with SFT cells, in vitro-activated peripheral blood lymphocytes from RA patients failed to trigger such arthritis, suggesting that pathogenic T cells might be concentrated in synovial fluid of RA patients. This, the first severe arthritis model mimicking RA induced by RA patients' T cells, is expected to provide important information about RA pathogenesis and a possible therapeutic approach.

Aged↗