Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
| ID | PMID | Title | PublicationDate | abstract |
|---|---|---|---|---|
| 1927064 | [Therapy of non-steroidal antirheumatic drug-induced gastrointestinal lesions with misopro | 1991 May | In a multicenter placebo-controlled double-blind study in patients with degenerative or inflammatory rheumatic diseases the prostaglandin analogue misoprostol, in a dose of 200 micrograms twice daily after meals, was administered for the treatment of NSAID-induced lesions and symptoms of the upper gastrointestinal tract. Treatment with an NSAID was continued. Misoprostol treatment was demonstrated to be clearly superior to placebo in respect of reduction of gastroduodenal lesions and gastrointestinal pain. In addition, the physician's global assessment of gastrointestinal complaints was also statistically significantly better. No difference between the groups was found with respect to antirheumatic action of the NSAIDs. | |
| 3030445 | A vertebrate interstitial collagenase inhibitor from bovine scapular cartilage: purificati | 1987 Apr 16 | A collagenase inhibitor was purified from bovine cartilage by a combination of gel filtration, ion exchange, concanavalin A-Sepharose affinity chromatography, and elution from preparative sodium dodecyl sulfate-polyacrylamide gels. The inhibitor was purified 370-fold and migrated as a single polypeptide with an Mr of 19,000 on SDS-polyacrylamide gels. It stained positively for carbohydrate with periodic acid-Schiff's reagent and bound to lectins, indicating that it is a glycoprotein. The inhibitory activity was stable to heating up to 60 degrees C and between pH 4 and 10. The inhibition of collagenase by the cartilage inhibitor could not be reversed by trypsin or mersalyl. The inhibitory activity did not require the presence of free sulfhydryl groups, and it could be removed from the cartilage extract by incubating with native collagen, suggesting that the inhibitor binds to collagen. The cartilage inhibitor was effective against human and mouse interstitial collagenases, but it did not inhibit trypsin or bacterial collagenase. | |
| 3495852 | Comparative studies of adherent rheumatoid synovial cells in primary culture: characterisa | 1987 | Primary cultures of adherent rheumatoid synovial cells contain variable proportions of fibroblasts, macrophages, and dendritic cells, as judged by morphological appearance. Comparative studies using various enzymic and histochemical staining procedures showed the dendritic cells to lack many of the characteristic features of macrophages, e.g. the failure to express HLA-DR (Ia) antigen. The dendritic cells and fibroblasts had several similarities, but differed to some extent in their nonspecific esterase activity, phagocytic and proliferative potential. As the proportions of dendritic cells and fibroblasts varied in relation to specific culture conditions, we examined the possibility that these morphologies might represent different functional states rather than distinct cellular origins. Using subcultured synovial fibroblasts with a uniform bipolar appearance, we have shown that exposure to interleukin-1 or mast cell products resulted in a transformation to dendritic morphology. This change in cell shape was prevented by the presence of indomethacin, but was subsequently achieved by the addition of exogenous PGE2. Thus it appears that the latter is the factor that modulates the morphological change of fibroblastic to dendritic cells. This study has also demonstrated the complete and reversible interchange of fibroblast/dendritic morphology, thereby confirming that these different shapes are manifest by the same cell. The changes in phenotypic expression associated with the dendritic appearance include increased production of collagenase, prostaglandin E, and nonspecific esterase, as well as an apparent inability to exhibit phagocytosis and to proliferate in culture. We conclude from our in vitro studies that the phenotypic behaviour of the synovial fibroblast (or synoviocyte) is very variable and dependent to a large extent upon local stimuli, but the identity and hierarchy of such stimulating and suppressive factors in relation to cellular interactions requires further study. | |
| 3005783 | Mechanisms of inflammation and leukocyte chemotaxis in the rheumatic diseases. | 1986 Mar | Understanding the mechanisms of inflammatory cell accumulation, as well as how such cells mediate tissue destruction, provides better insights into the pathogenesis and therapeutics of the rheumatic diseases. This article discusses the role of the inflammatory process in normal immune function, the mechanisms of inflammatory cell accumulation, and how the local accumulation of inflammatory cells can lead to the clinical signs and symptoms associated with rheumatic disorders. | |
| 2940684 | D-penicillamine: chemistry and clinical use in rheumatic disease. | 1986 May | The discovery of D-penicillamine and its uses in medicine are reviewed. Chemical-physical properties are discussed, and the molecular structure of D-penicillamine and several of its reaction products are illustrated. Examples of its three main types of biochemical reactions--sulfhydryl-disulfide exchange, thiazolidine formation, and metal chelation are included. Trials of D-penicillamine in RA patients are reviewed critically. The administration of the drug is discussed in detail, including dosages, clinical and laboratory responses, patterns of adverse side effects or toxicity, drug-induced autoimmune diseases, indications and contraindications, and the monitoring and management of patients. | |
| 1777012 | Immunological effects of high dose administration of anti-CD4 antibody in rheumatoid arthr | 1991 Aug | A phase I/II trial of the anti-CD4 monoclonal antibody (mAb) was undertaken in seven rheumatoid arthritis patients in order, (1) to investigate changes in clinical symptoms and possible side effects, and (2) to study the pharmacokinetics and to determine the dose required to achieve saturation of antibody binding sites on blood leucocytes. BL4mAb is a murine IgG2a which binds to the group 2B epitope of the V1 N terminal domain of the CD4 molecule. It inhibits syncitium formation by human immunodeficiency virus-infected cells. BL4 was administered by one hour-long intravenous infusion each day, for 10 days. Doses were steadily increased from 20 mg/d to 40 mg/d in the first three patients (group I) in an attempt to reach a serum antibody residual level sufficient to saturate CD4+ circulating cells. The three other patients (group II) received a dose of 40 mg/d during 10 consecutive days. One patient who presented chills and mild fever during the first BL4 infusion was not included in the analysis. No clinical side effects were observed in the six other BL4-treated patients. Clinical parameters of disease activity were improved within the first 14 days. Clinical improvement was still significant at day 30 in five patients, but at day 60, only the Ritchie index was still below pretreatment levels. Delayed type hypersensitivity reactions decreased in the three patients who exhibited positive reactions before BL4 administration. A transient drop in peripheral blood CD4+ lymphocyte counts occurred during each infusion in the first days of treatment. Pre-infusion CD4+ lymphocyte counts were moderately decreased within the first 8 days, but rose to pretreatment levels 3 days after the last infusion. BL4 residual levels in serum steadily increased to reach 8.0 micrograms/ml in group I and 9.8 micrograms/ml in group II. Saturation of BL4 binding sites was achieved after 2 days of treatment in all patients of group II but in only one of group I. Four out of six patients produced antibodies against the anti-CD4 mAb. Immunization appeared between days 12 and 50. This study shows that saturation of anti-CD4 mAb binding sites can be achieved by infusions of high doses (40 mg/d) of BL4 without clinical side effects. The results would encourage further placebo-controlled trials, since no definite conclusion can be drawn from the present study as regards clinical efficacy. | |
| 1816639 | [Circulating lymphocyte populations and B-cell differentiation in a young female patient w | 1991 Oct | Giant multicentric hyperplasia of the lymph nodes (GMHLN) is currently regarded as a disseminated form of angiofollicular lymphoid hyperplasia, or Castleman's disease. An immunologic study was carried out on a 24 year-old Caucasian woman who was admitted to hospital with generalised lymph node enlargement, jaundice and fever, and showed an excellent response to steroid therapy. No alterations were found in the lymphocytic subsets, the intrinsic B cell function or the T-B cooperative capability. These data disagree with the hypothesis than GMHLN is due to a deficiency of the T cell suppressive function with concomitant immunoglobulin over-production. | |
| 1711322 | Identification and characterization of opsonic fibronectin in synovial fluids of patients | 1991 Jun | A cofactor that selectively opsonizes particulate activators of the human alternative complement pathway and enhances their phagocytosis by human monocytes was identified in synovial fluids of patients with rheumatoid arthritis. The active material was present in fluids treated with protease inhibitors, was heat stable, and was unaffected by incubation with hyaluronidase. Chromatographic isolation of synovial fluid fibronectin by gelatin affinity and by immunoaffinity on antifibronectin monoclonal antibody BD4 yielded similar quantities of protein for each of 3 fluids. Synovial fluid proteins with the BD4 fibronectin epitope accounted for essentially all of the phagocytosis-enhancing activity and expressed this activity by opsonizing target activators. Additional chromatographic analyses of synovial fluid fibronectin with the BD4 epitope were carried out using Sepharose-bearing gelatin and 4 additional antifibronectin monoclonal antibodies. The opsonic materials were characterized as having 2 distinct fibronectin epitopes, which always mapped from the cell adhesive domain to the carboxyl-terminus of plasma fibronectin, but only rarely contained the gelatin binding domain. | |
| 1977391 | The comparative efficacy and toxicity of second-line drugs in rheumatoid arthritis. Result | 1990 Oct | We performed 2 metaanalyses of placebo-controlled and comparative clinical trials to examine the relative efficacy and toxicity of methotrexate (MTX), injectable gold, D-penicillamine (DP), sulfasalazine (SSZ), auranofin (AUR), and antimalarial drugs, the second-line drugs most commonly used to treat rheumatoid arthritis (RA). For the efficacy study, we applied a set of inclusion criteria and focused on trials which provided information on tender joint count, erythrocyte sedimentation rate, or grip strength. We found 66 clinical trials that contained 117 treatment groups of interest, and for each drug, we combined the treatment groups. For each outcome, results showed that AUR tended to be weaker than other second-line drugs. The results of the 3 outcome measures were synthesized into a composite measure of outcomes, and AUR was significantly weaker than MTX (P = 0.006), injectable gold (P less than 0.0001), DP (P less than 0.0001), and SSZ (P = 0.009) and was slightly, but not significantly, weaker than antimalarial agents (P = 0.11). We also found heterogeneity among antimalarial agents, in that patients treated with chloroquine did better than those treated with hydroxychloroquine. We found little difference in efficacy between MTX, injectable gold, DP, and SSZ. A power analysis showed that a trial should contain at least 170 patients per treatment group to successfully differentiate between more effective and less effective (e.g., AUR) second-line drugs. None of the reported interdrug comparative trials we reviewed were this large. For the toxicity study, our inclusion criteria captured RA trials which reported the proportion of patients who discontinued therapy because of drug toxicity and the total proportion who dropped out. We found 71 clinical trials that contained 129 treatment groups. The average proportion who dropped out and the average proportion who dropped out because of drug toxicity were computed for each drug. Overall, 30.2% of the patients in these trials dropped out; 50% of them did so because of drug toxicity. Injectable gold had higher toxicity rates (P less than 0.05) and higher total dropout rates (P less than 0.01) than any other drug; 30% of gold-treated patients dropped out because of side effects versus 15% of all trial patients. Antimalarial drugs and AUR had relatively low rates of toxicity; the rate for MTX was imprecise because of discrepancies between trials. Thus, of the commonly used second-line drugs, AUR is the weakest, and injectable gold is the most toxic. Agents introduced in the future will be compared with these drugs.(ABSTRACT TRUNCATED AT 400 WORDS) | |
| 3360803 | The complete primary structure of human matrix metalloproteinase-3. Identity with stromely | 1988 May 15 | We have determined the complete primary structure for human matrix metalloproteinase-3 (MMP-3), which has 477 residues including a 17-residue signal peptide. The result indicates that MMP-3 is identical with stromelysin (Whitham, S. E., Murphy, G., Angel, P., Rahmsdorf, H.-J., Smith, B. J., Lyons, A., Harris, T. J. R., Reynolds, J. J., Herrlich, P., and Docherty, A. J. P. (1986) Biochem. J. 240, 913-916). A striking result is that MMP-3 and collagenase are 54% identical in sequence, suggesting a common origin for the evolution of the two proteinases. We also show that in human synovial fibroblast cultures human recombinant interleukin-1 beta rapidly induces high levels of MMP-3 mRNA and, conversely, that retinoic acid or dexamethasone can suppress the MMP-3 mRNA levels. Similar results were obtained for human synovial collagenase mRNA. The data suggest that MMP-3 and collagenase expression are coordinately modulated in synovial fibroblast cultures. | |
| 2951351 | [Photosensitizing properties of nonsteroidal antirheumatic drugs in the photopatch test]. | 1987 Jan | The non-steroidal anti-inflammatory drugs, aspirin, carprofen, diclofenac, ketoprofen, piroxicam, and tiaprofenic acid, were tested in a standard photopatch test series. The routine irradiation dose was 15 J/cm2 UV-A; in most patients additional test series were exposed to non-erythematogenic doses of UV-B and a combination of UV-B and UV-A. In the photopatch test, there were reactions to tiaprofenic acid in 43 of 175 (24.6%), to carprofen in 21 of 86 (24.4%), to aspirin in 7 of 76 (9.2%), to piroxicam in 7 of 84 (8.3%), to diclofenac in 5 of 75 (6.7%), and to ketoprofen in 2 of 53 (3.8%). In 16 patients positive photopatch test results did not start to develop until after the 3rd test day (between day 7 and day 34). In some cases there were positive reactions within the non-irradiated control series. Most of the positive photopatch test reactions could be elicited by UV-A alone; in some cases, however, combined irradiation with UV-B plus UV-A was necessary to yield positive results; only rarely did positive reactions occur exclusively with UV-B. The high incidence of positive photopatch test reactions to non-steroidal anti-inflammatory drugs is a possible indication of a phototoxic action. However, in some cases a photoallergic pathomechanism seems probable with regard to the development of reactions after the 3rd test day, a high UV-sensitivity in the photopatch threshold test, and the results of the histological evaluation of test reactions in some patients.(ABSTRACT TRUNCATED AT 250 WORDS) | |
| 2138450 | Lymphocyte surface marker expression in rheumatic diseases: evidence for prior activation | 1990 Feb | Expression of major histocompatibility complex (MHC) class II and other lymphocyte activation markers on peripheral blood and synovial fluid T lymphocytes from patients with rheumatoid arthritis (RA), psoriatic arthritis, and Reiter's syndrome were measured and the mean fluorescence intensities of these antigens were assessed. Increased expression of MHC class II antigens of synovial fluid T lymphocytes is not unique to RA, though it is quantitatively greater on RA synovial fluid T cells. There was less expression of other lymphocyte activation markers (4F2, transferin receptor) and a marked discordance between the expression of these markers and the interleukin 2 receptor (IL2r). Synovial fluid T lymphocytes contain a subpopulation of larger cells expressing MHC class II and other lymphocyte activation antigens with the exception of the IL2r. Mean fluorescence intensity of CD3 and CD4 antigens on synovial fluid T lymphocytes was decreased in all three patient groups, suggesting prior in vivo exposure of synovial fluid T lymphocytes to an unknown antigen. | |
| 3009609 | Release of lymphokines after infection with Epstein Barr virus in vitro. II. A monocyte-de | 1986 May 15 | Epstein Barr virus (EBV)-infection of normal peripheral blood mononuclear cells (PBMC) in vitro induces IFN-alpha secretion from B cell and natural killer (NK) cell populations, and IFN-gamma secretion from T cells. IFN-gamma depends on prior elaboration of IL 2 and IL 1 that originates from monocytes and NK cells. PBMC from rheumatoid arthritis (RA) patients released moderately elevated levels of IFN-alpha (236 +/- 62 U/ml vs 168 +/- 34 in normals). In contrast, IFN-gamma was significantly lower in RA (88 +/- 34 U/ml vs 209 +/- 32) with an associated deficit in IL 2. A monocyte-dependent factor was shown to be responsible for this deficit, since monocyte depletion of RA cultures normalized the levels of IL 2 and IFN-gamma. Significantly lower levels of IL 1 activity were present in the supernatants of RA PBMC cultures as compared with normal cultures, and this was shown to be associated with presence of a nondialyzable IL 1 inhibitor. This inhibitor was capable of preventing the IL 1-dependent synthesis of IL 2 and IFN-gamma by normal PBMC. Exogenous IL 1 or IL 2 restored the deficient IFN-gamma secretion in RA PBMC. Thus, the deficient ability of RA lymphocytes to control EBV infection may be secondary to impairment of a monocyte-T cell interaction at the level of IL 1. | |
| 3088125 | Antibodies to La, Jo-1, nRNP and Sm detected by multi-track immunoblotting using a novel f | 1986 Jul 11 | The use of Western blotting or immunoblotting to detect autoantibodies in the serum of patients with autoimmune connective tissue diseases was investigated. An apparatus suitable for simultaneously screening 16 sera on immunoblots was used to show that a complex pattern of antibody binding polypeptides was present in whole HeLa cells. A simpler and readily interpreted pattern of binding was achieved using affinity-purified rabbit thymus antigens. Seventy-seven patients with systemic lupus erythematosus, 44 with primary Sjögren's syndrome and 50 normals were screened for anti-Sm, anti-La, anti-nRNP and anti-Jo-1 by immunoblotting and the results compared with those obtained by counterimmunoelectrophoresis and immunodiffusion. It was shown that both IgG and IgM antibodies must be analysed on immunoblots to detect the maximum number of positive sera, and that the immunoblot detects many anti-La sera which do not form precipitins. | |
| 1976464 | In vitro production of interferon-gamma by peripheral blood from patients with Graves' dis | 1990 Oct | The production of interferon-gamma (IFN-gamma) by peripheral blood mononuclear cells (PBMC), CD4 cells, or CD8 cells in response to interleukin-2 (IL-2) stimulation has been studied; the samples were obtained from 12 healthy control subjects, 19 patients with Graves' disease (10 hyperthyroid and nine euthyroid), 13 patients with Hashimoto's thyroiditis (four hypothyroid and nine euthyroid), and 15 patients with rheumatoid arthritis (11 active and four inactive). A dose of IL-2 (25 U/ml) was utilized to induce IFN-gamma by PBMC from all four groups. The incremental increase in IFN-gamma values (with IL-2 stimulation minus without stimulation) was significantly less in PBMC from patients with Graves' disease, Hashimoto's thyroiditis, and rheumatoid arthritis than that in PBMC from control subjects. The values from PBMC in patients with Graves' disease in a euthyroid state were below normal but greater than those from patients with Graves' disease in a hyperthyroid state. The incremental increase in IFN-gamma values from Graves' disease PBMC correlated with the serum TSH values (r = 0.622, P less than 0.01), but not with thyroid autoantibodies (anti-thyroid microsomal antibodies, anti-thyroid microsomal antibodies, nor TSH-binding inhibitory immunoglobulin activities). The incremental increase in IFN-gamma from PBMC from both control subjects and Graves' disease was correlated with that from CD4 cells (r = 0.711, P less than 0.01), but not with that from CD8 cells. The production of IFN-gamma in response to IL-2 from PBMC in Graves' disease correlated inversely with thyroid function, appearing to reflect the very effect of hyperthyroidism in this process. The precise explanation of these phenomena remains unclear. The decreased response of IFN-gamma to IL-2 stimulation by PBMC from patients with Graves' disease, Hashimoto's thyroiditis, and rheumatoid arthritis seems to be a non-specific phenomenon occurring in both organ specific autoimmune disease and systemic autoimmune disease. It may be due to a down-regulation in autoimmune disease of CD4 cells in response to IL-2, a decreased level of IL-2 cellular receptors or a decreased receptor affinity, associated increased soluble IL-2 receptors, or a defect of the intra-CD4 cellular IL-2 signal to produce or release IFN-gamma in the conditions studied. | |
| 2319519 | Sjögren's syndrome in systemic lupus erythematosus. | 1990 Feb | Sixty unselected consecutive patients with systemic lupus erythematosus (SLE) were prospectively evaluated for evidence of Sjögren's syndrome. This was diagnosed in the patients whose minor labial salivary gland biopsy was graded greater than or equal to 3 (according to Chisolm and Mason), who also had keratoconjunctivitis sicca (positive rose bengal eye test) and/or xerostomia (subjective xerostomia and decreased stimulated parotid flow rate). Lip biopsy revealed focal round cell infiltration compatible with a greater than or equal to 3 grade in 11 patients, minimal perivascular infiltration in 21 patients and no infiltration in 28. In the positive biopsy group (greater than or equal to 3 grade) subjective xerophthalmia, decreased parotid flow rate, parotid gland enlargement, lymphadenopathy, presence of rheumatoid factor and anti-La (SSB) antibodies were significantly commoner than in the others. Of the 11 patients of this group, 5 had keratoconjunctivitis sicca which sufficed for the diagnosis of Sjögren's syndrome, suggesting a prevalence of 8.3% in our population with SLE. In these individuals subjective xerophthalmia (40%), positive Schirmer's I eye test (60%), decreased parotid flow rate (80%), parotid gland enlargement (80%) and presence of rheumatoid factor (80%) and anti-La (SSB) antibodies (80%) were significantly more frequent than in the remaining patients, whereas significant differences regarding other features of SLE were not observed. Our results suggest that Sjögren's syndrome in SLE is relatively rare and usually mild. Furthermore, it may present more similarities to primary Sjögren's syndrome than to secondary Sjögren's syndrome accompanying rheumatoid arthritis. | |
| 2165196 | The role of gamma delta T cells in the normal and disordered immune system. | 1990 May 17 | A small population of T cells does not express the conventional T cell receptor characterized by the alpha and beta polypeptide chains (TCR alpha beta) but instead, two polypeptides termed gamma and delta (TCR gamma delta). This alternative receptor is able to recognize antigen. It appears early in T cell ontogeny, but its role in the thymus prior to the availability of TCR alpha beta remains unclear. In selected sites such as skin or gut TCR gamma delta predominates in mice which might suggest a role of gamma delta T cells in the first line of defense against infection. gamma delta T cells secrete lymphokines and display cytotoxic activity. However, their activation requirements may differ from what is known for alpha beta T cells since MHC-nonrestricted and also CD4 and CD8 negative gamma delta T cells have been described. Preferential activation by mycobacterial antigens possibly indicates a special repertoire of the gamma delta T cells. In various diseases slightly increased numbers of gamma delta T cells were found, but these preliminary studies have not yet provided evidence for a major pathogenetic role of gamma delta T cells. | |
| 3263464 | Cytokines in chronic inflammatory arthritis. I. Failure to detect T cell lymphokines (inte | 1988 Nov 1 | Because previous studies showed low levels of IFN-gamma in rheumatoid arthritis (RA) synovial fluid (SF) and synovial tissue (ST) explant supernatants, we assayed RA SF and ST for IL-2 and IL-3-like activity. Using an IL-2 dependent murine CTLL line, 6 of 14 RA SF caused increased thymidine uptake (greater than three times control). The activity was distinct from IL-2 because it was not blocked by antibody to IL-2-R. In addition, IL-2 was not detected (less than 50 pg/ml) in 16 joint samples using an ELISA. Multi-colony-stimulating factor (CSF) activity was measured using two assays that can detect murine IL-3 (mast cell proliferation, and bone marrow CSF). In the mast cell assay, [3H]TdR uptake was 493 +/- 67 cpm for medium, 2,910 +/- 329 cpm in the presence of RA SF (p less than 0.001), 1,246 +/- 156 cpm in the presence of SF from patients with seronegative spondyloarthropathies (p less than 0.001), and 736 +/- 100 cpm in the presence of osteoarthritis SF (p greater than 0.1). In the CSF assay, four of five RA SF and five of five RA ST induced colony formation from bone marrow nonadherent cells. Macrophage colonies were most common, although mixed colonies and granulocytes were occasionally observed. The multi-CSF activity in RA is not due to IL-3 since human rIL-3 was not active in either murine assay, and IL-3 mRNA was not detected in RA synovium. Sephadex column chromatography of RA SF revealed that the mast cell growth factor (approximately 6 x 10(3) mol wt) and the CSF (approximately 40 and 100 x 10(3) mol wt) are distinct. The colony-stimulating aspect of the "IL-3-like" activity in RA SF is likely due to CSF-1 because it is the appropriate mol wt and because the activity was neutralized by specific anti-CSF-1 antibody. Finally, an RIA detected 1.6-25 ng/ml of CSF-1 in RA SF and ST and CSF-1 mRNA was detected in four of five RA synovial tissue samples tested. | |
| 3308228 | Expression of MHC class I determinants on erythrocytes of SLE patients. | 1987 Aug | Strong expression of MHC Class I determinants had been observed on the erythrocytes of three genetically C4 deficient patients who all had SLE. In a study of 35 other SLE patients who were not C4 deficient, 30 showed a marked increase in the expression of MHC Class I on their erythrocytes. There was a correlation between the expression of erythrocyte Class I and disease activity. The polymorphic HLA determinants were detected by haemagglutination with human cytotoxic antisera from untransfused pregnant women. A shared monomorphic epitope of HLA-A, -B and -C, and beta 2-microglobulin were detected by haemagglutination with monoclonal antibodies. A monoclonal antibody for a monomorphic epitope on MHC Class II alpha and beta chains did not react. Erythrocytes from a group of RA patients and a group of normal controls had moderate and low expression respectively. We suggest that MHC Class I may be induced on erythrocytes maturing in a milieu containing mediators derived from activated cells of the immune system. Aberrant tissue expression of MHC antigens may be more widespread than has been previously recognized in diseases mediated by immune mechanisms. | |
| 3034241 | Inhibition of human neutrophil collagenase by gold(I) salts used in chrysotherapy. | 1987 Apr 14 | Six gold(I) salts, some of which are used as drugs in chrysotherapy, are shown to be inhibitors of two forms of human neutrophil collagenase. The IC50 values vary over six orders of magnitude, the lowest being 3.5 nM for Myocrisin. Thus, inhibition is greatly affected by the identity of the ligands to the gold(I) atom. The inhibition of collagenase by these gold(I) salts may be a partial basis for their antiarthritic action. |