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ID PMID Title PublicationDate abstract
8381986 Relationship between autoantibodies and clinical parameters in Sjögren's syndrome. 1993 Glandular function as estimated by salivary function scintigraphy and extraglandular manifestations were compared among 174 Sjögren's syndrome (SS) patients according to their anti-Ro/SSA, anti-La/SSB, and anti-U1RNP autoantibody status, to clarify the relationship between these autoantibodies and clinical parameters in SS. These antibodies were detected by RNA-immunoprecipitation. Anti-La/SSB or only anti-Ro/SSA antibody was common in 84 primary SS (P-SS) patients, whereas the frequency of only anti-U1RNP was high in 90 secondary SS (S-SS) patients, especially in those with systemic lupus erythematosus (SLE). Antibody-negativity was common in SS with rheumatoid arthritis and was also found in 33% of P-SS. In P-SS, salivary gland dysfunction and parotid swelling were severe in patients who had serological abnormalities with anti-Ro/SSA and with or without anti-La/SSB. They were mild in antibody-negative patients who had mild extraglandular symptoms and in patients with only anti-U1RNP antibody who had Raynaud's phenomenon, pulmonary fibrosis, and later disease onset. P-SS patients positive for both anti-Ro/SSA and anti-U1RNP had SLE-like features. SS could be classified clinically according to these autoantibodies.
7638179 Autoantibodies to calpastatin (an endogenous inhibitor for calcium-dependent neutral prote 1995 Aug 1 We identified an autoantibody that reacts with calpastatin [an inhibitor protein of the calcium-dependent neutral protease calpain (EC 3.4.22.17)]. In early immunoblot studies, sera from patients with rheumatoid arthritis (RA) recognized unidentified 60-, 45-, and 75-kDa proteins in HeLa cell extracts. To identify these autoantigens, we used patient sera to clone cDNAs from a lambda gt11 expression library. We isolated clones of four genes that expressed fusion proteins recognized by RA sera. The 1.2-kb cDNA insert (termed RA-6) appeared to encode a polypeptide corresponding to the 60-kDa antigen from HeLa cells, since antibodies bound to the RA-6 fusion protein also reacted with a 60-kDa HeLa protein. The deduced amino acid sequence of the RA-6 cDNA was completely identical with the C-terminal 178 amino acids of human calpastatin except for one amino acid substitution. Patient sera that reacted with the RA-6 also bound pig muscle calpastatin, and a monoclonal antibody to human calpastatin recognized the RA-6 fusion protein, confirming the identity of RA-6 with calpastatin. Moreover, the purified RA-6 fusion protein inhibited the proteolytic activity of calpain, and IgG from a serum containing anti-calpastatin antibodies blocked the calpastatin activity of the RA-6 fusion protein. Immunoblots of the RA-6 product detected autoantibodies to calpastatin in 57% of RA patients; this incidence was significantly higher than that observed in other systemic rheumatic diseases, including systemic lupus erythematosus (27%), polymyositis/dermatomyositis (24%), systemic sclerosis (38%), and overlap syndrome (29%). Thus, anti-calpastatin antibodies are present most frequently in patients with RA and may participate in pathogenic mechanisms of rheumatic diseases.
8310085 Arthritis-associated syndromes. 1993 Dec There are a number of diseases characterized by inflammatory arthropathy that, although not as commonly seen as rheumatoid arthritis, often present to the family physician as difficult diagnostic problems. The diagnosis is frequently most difficult during the early course of these diseases. During recent years, new and altered concepts have arisen regarding both diagnostic and therapeutic management of this challenging group of arthropathies. This article presents a review of the more common arthritis-associated syndromes with emphasis on the differential diagnosis and medicinal therapeutics.
8075862 AT1 receptor characteristics of angiotensin analogue binding in human synovium. 1994 Jun 1. Angiotensin II (AII) reduces blood flow, modulates vascular remodelling and is a growth factor. Human inflammatory arthritides are characterized by synovial hypoperfusion, hypoxia and proliferation. We aimed to localize and characterize receptors for AII in human synovium. 2. We used quantitative in vitro receptor autoradiography with [125I]-(Sar1, Ile8)AII and [125I]-AII on human synovium from patients with chondromalacia patellae, osteoarthritis and rheumatoid arthritis. 3. [125I]-(Sar1, Ile8)AII and [125I]-AII bound to similar sites on synovial blood vessels, lining cells and stroma. Binding to microvessels (< 100 microns diameter) was more dense than to arteriolar media, and vascular binding was more dense than that to lining cells and stroma. 4. Microvessels and arterioles which displayed angiotensin converting enzyme-like immunoreactivity also displayed specific binding of [125I]-(Sar1, Ile8)AII. 5. Specific binding of [125I]-(Sar1, Ile8)AII to each structure was completely inhibited by 10 microM dithiothreitol and was inhibited by unlabelled ligands with the rank order of potency (Sar1, Ile8)AII > AII > losartan = SKF108566 > PD123319 indicating an AT1 subclass of angiotensin receptor. 6. GTP gamma S (1 microM) abolished specific binding of [125I]-AII and abolished the high affinity component of the binding inhibition curve for AII against [125I]-(Sar1, Ile8)AII, indicating G protein coupling. 7. The distribution of [125I]-(Sar1, Ile8)AII binding sites was similar in all disease groups and no significant differences in binding densities, affinities or specificities were observed between disease groups. 8. Locally generated AII may act on synovial AT1 receptors to modulate synovial perfusion and growth. Specific AT1 receptor antagonists should help elucidate the role of angiotensins in human arthritis.
1512757 Bucillamine inhibits T cell adhesion to human endothelial cells. 1992 Jul We investigated the ability of bucillamine [N-(2-mercapto-2-methyl-propionyl)-L-cysteine] to prevent T cell adhesion to endothelial cells (EC) isolated from human umbilical vein. When EC were pretreated with bucillamine, T cell binding to the EC was suppressed in a dose dependent fashion. The T cells could bind preferentially to recombinant interferon-gamma (rIFN-gamma) treated EC compared with untreated EC. Bucillamine could also suppress T cell binding to rIFN-gamma treated EC as well as untreated EC. Addition of copper sulfate to bucillamine decreased significantly the percent T cell adhesion to the EC compared with bucillamine alone. The magnitude of inhibition by bucillamine and copper sulfate was similar in EC treated with rIFN-gamma as well as in untreated EC. H2O2 also inhibited the T cell binding to both untreated and rIFN-gamma treated EC. The inhibitory effects of bucillamine with or without copper sulfate on T cell binding to EC were abolished completely by catalase but not by superoxide dismutase. Our results suggest that hydrogen peroxide generated by bucillamine, with or without copper sulfate, inhibits T cell binding to EC. We believe, therefore, that bucillamine may suppress inflammation, such as that in rheumatoid synovitis, by reducing the emigration of chronic inflammatory cells from capillaries into tissue.
8058775 Nonpeptide ligands for human gamma delta T cells. 1994 Aug 16 gamma delta T cells respond to a variety of microbial pathogens and transformed cells. Their limited receptor repertoire and activation by mycobacterial antigens resistant to proteases suggest that they may recognize nonpeptide antigens. We have tested a variety of nonpeptide molecules for stimulation of human gamma delta T cells. Synthetic alkyl phosphates, particularly monoethyl phosphate (MEP), selectively activated gamma delta T cells and stimulated their proliferation in vitro. All gamma delta T cells stimulated by MEP expressed V gamma 2/V delta 2 receptors. The purified natural ligand of mycobacteria is chemically similar to, though distinct from, MEP and contains a phosphate residue that is critical for biological activity. Recognition and expansion of a specific T-cell receptor-bearing population to non-peptide ligands is unprecedented among T cells. We suggest that MEP mimics small natural ligands capable of expanding one subset of gamma delta T cells and that this recognition of nonpeptide antigens may play an important role in human immunity to pathogens.
8694577 Interleukin-4 inhibits prostaglandin E2 production by freshly prepared adherent rheumatoid 1996 Jun OBJECTIVE: To characterise the effect of interleukin-4 (IL-4) on the biosynthesis of cyclo-oxygenases I (COX I) and II (COX II), the rate limiting enzymes of the synthesis of prostaglandin E2 (PGE2), in freshly prepared rheumatoid synovial cells. METHODS: Adherent synovial cells were obtained from rheumatoid synovium by collagenase digestion. The concentrations of PGE2 in culture supernatants were determined by enzyme linked immunosorbent assay. The protein and mRNA concentrations of COX I and COX II were determined by Western blotting and reverse transcription polymerase chain reaction, respectively. RESULTS: Freshly prepared synovial cells produced large amounts of PGE2. They also showed increased gene expression of COX I and COX II, and synthesised these proteins. IL-4 had suppressive effects on the production of PGE2 by untreated or lipopolysaccharide (LPS) stimulated synovial cells. In addition, IL-4 inhibited the biosynthesis of COX II at the mRNA level. In contrast, it did not modify the protein concentration of COX I. In tests of cell specificity, IL-4 did not reduce the mRNA concentration of COX II in interleukin-1 alpha (IL-1 alpha) stimulated cultured synovial fibroblasts at passages 3-6, but it reduced considerably the mRNA concentrations of COX II in an LPS or IL-1 alpha stimulated U937 monocyte/macrophage cell line. CONCLUSIONS: These results suggest that IL-4 might inhibit overproduction of PGE2 in rheumatoid synovia via selective inhibition of the biosynthesis of COX II, and that this inhibition might be specific to macrophage-like synovial cells.
7526808 Interleukin 4 increases human synovial cell expression of VCAM-1 and T cell binding. 1994 Sep OBJECTIVE: The effects were studied of interleukin 4 (IL-4) on T cell-synovial cell adhesion and on the expression of adhesion molecules on the surface of synovial fibroblast-like cells. METHODS: The adhesion of T cells toward the synovial cells were measured by 51chromium-labelled adhesion assay. The expression of adhesion molecules on synovial cells were analysed by flowcytometry. RESULTS: Stimulation of synovial cells with IL-4 increased T cell-synovial cells adhesion in a time- and dose-dependent manner. IL-4 considerably enhanced the expression of VCAM-1 on the surface of synovial cells, but not the expression of ICAM-1 and ELAM-1. The combination of IL-1 beta and IL-4 had no effect on the expression of ICAM-1 or VCAM-1 on the surface of synovial cells. The increased adhesion of T cells to IL-4 stimulated synovial cells was inhibited significantly by adding anti-VCAM-1 or anti-CD29 monoclonal antibody. Furthermore, anti-VLA-4 alpha or the combination of anti-VLA-4 alpha and anti-VCAM-1 antibodies blocked completely T-cell binding to IL-4 stimulated synovial cells. CONCLUSIONS: These results suggest that the increased adhesion of T cells to IL-4-stimulated synovial cells is mediated by VLA-4/VCAM-1 pathway.
7767779 Reactive oxygen species and iron--a dangerous partnership in inflammation. 1995 Feb Cells of nearly all forms of life require well-defined amounts of iron for survival, replication and expression of differentiated processes. It has a central role in erythropoiesis but is also involved in many other intracellular processes in the tissues of the body. It is the fourth most abundant element in the Earth's crust and the most abundant transition metal in living organisms for which its characteristic chemistry endows it with a series of properties enabling it to fulfil certain biological reactions especially those involving redox mechanisms. It is involved in the transport of oxygen, in electron transfer, in the synthesis of DNA, in oxidations by oxygen (O2) and hydrogen peroxide (H2O2) and in many other processes maintaining normal structure and function of virtually all mammalian cells. Because an iron atom can exist in two valency states, ferrous and ferric, iron became the primordial partner of oxygen in evolution. However, as de Sousa et al. (1989) state, such long standing partnerships have to use protective devices to ensure that the toxicity of neither partner is expressed in the presence of the other. Here, we discuss this dangerous partnership and its relevance to inflammation. The main themes of this review are the known roles of iron in the generation of reactive oxygen intermediates and new developments, including iron and transcription and the reaction of iron with nitric oxide. We also consider the widening recognition of the importance of oxygen metabolites in hypoxia-reperfusion injury and disease of the skin and joint.
1643162 Lymph node histology simulating T-cell lymphoma in adult-onset Still's disease. 1992 Jul A patient with adult-onset Still's disease (AOSD) underwent lymph node biopsy as part of initial evaluation for fever of unknown origin. The lymph node histology showed a massive, diffuse immunoblastic hyperplasia, simulating T-cell lymphoma. This nodal histology differs from rheumatoid arthritis, where mostly a follicular B-cell reaction predominates. Evaluating fever of unknown origin when one is unacquainted with this massive immunoblastic hyperplasia can lead to the wrong diagnosis of T-cell lymphoma in patients with AOSD.
7946269 Identification of a soluble Fc gamma-binding molecule (annexin II) in human serum using a 1994 Sep We have previously produced a monoclonal antibody (mAb), B1D6, reactive with a 37 kD placental IgG Fc-binding molecule (FcR), recently identified as annexin II. Annexin II is an intracellular molecule found in several cell types, including endothelium and monocytes. Since soluble Fc-binding molecules are of importance in the regulation of the immune response, we have now used B1D6 in a competitive ELISA to study levels of soluble annexin II in human sera. Soluble annexin II was detected in all sera studied. The highest levels were observed in patients with infectious mononucleosis. Gel filtration of sera revealed annexin II in fractions corresponding to a molecular weight of 40-60 kD. In Western blot analysis a molecule of approximately 37 kD was found. The pI of soluble annexin II was about 7.5-8 as demonstrated by chromatofocusing. Annexin II belongs to a family of phospholipid-binding molecules involved in anti-inflammatory responses, and elevated levels of annexin II in serum may be important for the suppression of an immune response.
7692987 Interacting monocytes and synoviocytes induce adhesion molecules by a cytokine-regulated p 1993 Aug Monocytes/macrophages and synovial fibroblast-like cells are in intimate contact in the synovium and are believed to play a critical role in the development of rheumatoid arthritis. We investigated the effects of monocyte-synoviocyte interactions in vitro on cytokine release and the expression of adhesion molecules. Using a sensitive Western blot assay, we found that VCAM-1 and ICAM-1 expression were up-regulated in synoviocytes following coculture. The interaction also resulted in the accumulation of TNF and IL-6, but not IFN-gamma in the culture medium. Culture supernatant from monocyte-synoviocyte samples effectively induced adhesion molecules in synoviocytes. Anti-TNF partially inhibited the increase in VCAM-1 and ICAM-1 expression, indicating that TNF in part mediates VCAM-1 and ICAM-1 expression. Interestingly, the induction of cytokines and adhesion molecules did not require cell contact between monocytes and synoviocytes, suggesting cell communication via soluble factors. T cell cytokines enhanced the induction of adhesion molecules induced by the monocyte-synoviocyte interaction. IFN-gamma and IL-4, which are produced by distinct T helper subsets, had differential effects on monocyte-synoviocyte interactions. IFN-gamma had a minimal effect on VCAM-1 expression by synovial fibroblasts, but synergized with monocytes to dramatically up-regulate ICAM-1 expression. IL-4 had no effect on ICAM-1 expression but enhanced monocyte-induced expression of VCAM-1. Our results demonstrate that the up-regulation of adhesion molecules following monocyte-synoviocyte interactions is mediated by soluble factors and can be regulated by specific T cell cytokines.
8023009 [Still's disease in the adult]. 1994 May The adult Still's disease (ASD) is an uncommon inflammatory systemic disorder which affects the young adult. It is characterized by high spiking fever, vanishing rash, oligopolyarthritis, neutrophilic leucocytosis, negative titers for rheumatoid factor and antinuclear antibodies. Polyserositis, sore throat, uveitis are sometimes present and in one third of the cases it is possible to find hepato-splenomegaly with lymph node enlargement. G. Still first described the disease in child, in 1897, and in the adult it was recognized as a nosologic entity more than 70 years later. The ASD diagnosis is difficult and it is possible after the exclusion of many other diseases. Clinical manifestation are all nonspecific. In particular the presence of adenopathy, hepato-splenomegaly may suggest the possibility of a malignant lymphoma. Important exclusions include many other diseases such as the rheumatic fever, periodic fever, Lyme disease. At the same time a probable diagnosis of ASD should be considered in all the cases of high fever with rash, arthritis, neutrophilic leucocytosis or in the cases of fever of unknown origin (FUO). The prognosis is considered overall benign. The disease is usually sensible to salicylate treatment, even but the association with corticosteroids or, sometimes, with cytotoxic therapy is often required.
1616362 Follow up study of labial salivary gland lesions in primary Sjögren's syndrome. 1992 Jun Labial salivary gland biopsy samples were taken from 27 patients with primary Sjögren's syndrome (SS), 10 with rheumatoid arthritis (RA) and secondary SS, and four normal control subjects on two occasions at intervals of more than one year. In the former group of patients, eight of the nine initially negative analyses were positive on the second sample, whereas two of the seven patients with RA and secondary SS were negative for the first sample and then positive for the second. In primary SS, the mean (SD) variation of the focus score was 1.7 (2.6) and that of salivary duct infiltration 0.2 (0.7). The former correlated well with the latter.
1603198 Sjögren's syndrome in relation to other autoimmune diseases. 1992 Apr Autoimmune diseases can be divided into primary autoimmune diseases, in which the immune system is over-reactive, leading to an oligoclonal B cell stimulation, and secondary autoimmune diseases, in which the immune system is completely normal but some autoantigens are slightly altered, and are thus considered to be foreign. Sjögren's syndrome probably has characteristics of both types of autoimmune disease. The primary autoimmune diseases can be divided into organ-specific autoimmune diseases like thyroiditis, gastritis and adrenalitis, and generalised autoimmune diseases, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis. Sjögren's syndrome has characteristics of both types of primary autoimmune disease, and therefore occupies a central position among the other autoimmune diseases. The focal position of the disease in the present issue of The Netherlands Journal of Medicine is because of the symposium organized for the occasion of the fifth anniversary of the "Dutch Association of Patients with Sjögren's Syndrome", of which this issue is the report.
7608649 Hypertension in cyclosporin A-treated patients is independent of circulating endothelin le 1995 Jul OBJECTIVES: To measure blood pressure (BP), plasma endothelin-1 (ET-1), atrial natriuretic peptide (ANP), antidiuretic hormone (ADH) and aldosterone (ALDO) concentration, and plasma renin activity (PRA) in patients treated with a low-dose cyclosporin A (CyA). DESIGN: An open study of patients with rheumatoid arthritis (RA) or palmoplantar pustulosis (PPP). SETTING: Out-patient clinics at the Central Hospital of Jyväskylä and Helsinki University Central Hospital. SUBJECTS: CyA was given to 25 patients with RA and to 10 patients with PPP. INTERVENTION: RA patients were given CyA at a dose of 2.5 +/- 0.13 mg kg-1 body weight (BW) to 3.47 +/- 0.79 mg kg-1 BW (mean values +/- SD) at the start of the study and after 6 months, respectively, and the CyA dose was 2.67 +/- 0.13 mg kg-1 BW decreasing to 2.07 +/- 0.96 mg kg-1 (P < 0.001) after 4 months in PPP subjects. RESULTS: Systolic (sBP) and diastolic blood pressure (dBP) increased from 127.8 +/- 13.6/79.7 +/- 8.4 mmHg to 140.0 +/- 19.8/83.8 +/- 9.7 mmHg during the study (P < 0.03). Plasma ET-1, ANP, ALDO and ADH concentration and PRA did not change during 4 to 6 months of CyA treatment. The plasma ANP concentration was constantly higher in CyA-treated RA patients (112 +/- 87 ng 1-1 to 118 +/- 78 ng 1-1) than in PPP patients (37.3 +/- 26 ng 1-1 to 47.7 +/- 39.9 ng 1-1; P < 0.02). The serum creatinine concentration remained within the normal range, but increased from baseline (76.7 +/- 11.9 mumol 1-1), to 90 +/- 15.4 mumol 1-1 (p < 0.001). The serum magnesium concentration decreased significantly (P < 0.005) after 6 months of CyA treatment in RA patients. No correlation was found between serum creatinine and plasma ET-1 concentration. CONCLUSIONS: Increased blood pressure during CyA treatment was independent of circulating ET-1 levels. A low dose of CyA did not induce increased ET-1 synthesis as judged from plasma samples. The high plasma ANP level observed in RA patients could be due to fluid retention caused by concomitant treatment with non-steroid anti-inflammatory drugs. Fluid retention and decreased magnesium levels could also be involved in the development of hypertension in CyA-treated subjects.
9001833 Comparison of electromotive drug administration with ketorolac or with placebo in patients 1996 Nov This study was undertaken to assess the efficacy of ketorolac compared with placebo when delivered by electromotive drug administration (EMDA) in patients with pain from rheumatic disease. In EMDA, or iontophoresis, a low-intensity electric current is applied over the skin to deliver medication into body tissues. Although EMDA has been used to treat patients with various diseases, controlled studies are lacking in patients with rheumatic disease. This double-masked study included 60 patients (43 women and 17 men) aged 31 to 80 years with the following conditions: 12, epicondylitis; 30, scapulohumeral periarthritis; 10, gonalgia; and 8, metatarsalgia. They were divided randomly by a physician into 2 groups of 30 patients each for 5 sessions of active treatment (30 mg of ketorolac) or placebo (5 mL of normal saline). Treatment took place every other day for 20 minutes. Immediately before and after the five treatment sessions and 7 days after treatment ended, both patient and physician measured the degree of pain using a categoric scale (no pain, slight pain, intermediate pain, strong pain, and very strong pain) and evaluated pain intensity using the Scott and Huskisson Visual Analogue Scale (VAS). Seven days after treatment ended, both physician and patient judged the result of treatment using a second categoric scale (no improvement or intermediate, good, or very good result). Both ketorolac and placebo provided immediate, significant pain relief when delivered by EMDA, but only those patients receiving ketorolac experienced a further reduction in pain 7 days after treatment; those receiving placebo experienced a slight increase in pain. VAS values differed significantly between the two groups. Poor results (no improvement) were significantly higher in the placebo-treated group, while good results were significantly higher in the ketorolac-treated group. No patient reported any adverse effects during treatment. This study demonstrates that ketorolac relieves pain when delivered by EMDA and offers longer-lasting pain relief than does placebo.
7907476 T cell influence on superantigen-induced arthritis in MRL-lpr/lpr mice. 1994 Jan OBJECTIVE: To define the influence of the T cell receptor (TCR) and the lpr autoimmune gene on the induction and progression of superantigen-induced arthritis in V beta 8 transgenic MRL-lpr/lpr mice. METHODS: The time to onset and the extent of synovial hyperplasia after the induction of arthritis by intraarticular injection of staphylococcal enterotoxin B (SEB) were compared in mice having T cells that bear the V beta 8 transgene alone (V beta 8 TCR transgenic MRL-+/+), the lpr gene without the V beta 8 gene (nontransgenic MRL-lpr/lpr), both the V beta 8 gene and the lpr gene (V beta 8 transgenic MRL-lpr/lpr), or neither gene (nontransgenic MRL-+/+). Synovial hyperplasia was compared in SEB-injected V beta 8 transgenic MRL-lpr/lpr mice after treatment with cyclosporin A (CSA), anti-V beta 8 and anti-CD4 monoclonal antibodies, and in V beta 8 transgenic MRL-lpr/lpr mice after injection of a non-V beta 8-reactive superantigen, staphylococcal enterotoxin A (SEA). RESULTS: At day 30, increased synovial cells were observed in all SEB-treated mice, but the increase was greatest in the V beta 8 transgenic MRL-lpr/lpr mice. T cell involvement was indicated by the inability of either heat-denatured SEB or SEA to induce severe arthritis, the reduction in the severity of the arthritis on systemic treatment with CSA or anti-V beta 8, and the correlation of synovial hyperplasia with in vitro SEB reactivity of T cells. CONCLUSION: These observations suggest that superantigens can induce chronic arthritis and that the induction and progression of the arthritis requires an underlying T cell defect in anergy induction in addition to exposure to the superantigen.
8581407 Anti-epithelial (anti-A549) antibodies: their nature, specificity and relevance to transpl 1995 Sep Several studies have addressed the possible importance of anti-epithelial cell antibodies in kidney transplantation using the A549 cell line as an in vitro model. In this paper we report our results using for the first time an enzyme-linked immunosorbent assay (ELISA) to detect the anti-A549 cell antibodies. Sera from 129 kidney transplant patients were tested for IgM anti-epithelial cell antibodies directed against the A549 cell line prior to transplantation; only three sera were positive (2.3%). 101 of these patients were then followed-up post-transplantation; sera were collected routinely at 2, 6 and 12 weeks and at the time of rejection episodes. All samples were also tested for cytomegalovirus (CMV) IgM antibodies. Sixteen patients developed anti-A549 IgM antibodies, and there was no correlation with acute graft rejection. Anti-epithelial antibodies showed no binding to sections of normal kidney or biopsies of rejected kidneys. Eleven patients were positive for anti-CMV IgM antibodies. In nine cases both IgM anti-A549 and IgM anti-CMV antibodies were found, which was a highly significant association (p < 0.001). Analysis of A549 cellular proteins by immunoblotting gave evidence for the presence of CMV polypeptides in the cell lysate. Electron-microscopic examination of A549 cell preparations revealed intracellular particles which were compatible in size with CMV. Polymerase chain reaction analysis confirmed the presence of a specific CMV DNA sequence in A549 cells of several batches from different sources. Our data strongly suggest that the A549 cell line used in several published reports is infected with CMV and that in the majority of cases the anti-A549 'anti-epithelial' antibodies found in renal transplant patients are anti-CMV antibodies.
8828953 High dose intravenous immunoglobulin therapy for rheumatic diseases: clinical relevance an 1996 May The actual efficacy and applicability of high dose intravenous immunoglobulin (IVIG) therapy in the rheumatic disorders is still being debated. In the last few years clinical results have become available on a large number of patients, and efforts have been devoted to experimental studies of the mechanism of action of IVIG. However, the results of controlled clinical trials will be crucial to indicate stricter guidelines and directions for future clinical and experimental research. IVIG is of major value in Kawasaki disease and in severe lupus-associated thrombocytopenia. Its possible benefits are also remarkable in refractory dermatomyositis and probably in some patients with the antiphospholipid syndrome and recurrent miscarriages despite standard treatment. At present, the role of IVIG therapy remains controversial in lupus nephritis and in systemic vasculitis, while it does not seem to be effective in rheumatoid arthritis.