Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
| ID | PMID | Title | PublicationDate | abstract |
|---|---|---|---|---|
| 3930100 | Enzyme linked immunosorbent assay for lactoferrin. Plasma and tissue measurements. | 1985 Sep 16 | Highly purified lactoferrin was obtained from human breast milk by sequential use of affinity chromatography and isoelectric focusing. IgG antibody to purified lactoferrin was used to develop a sensitive and reproducible enzyme linked immunosorbent assay. Characteristics of the assay included linearity over a wide range of lactoferrin concentration (3.125-200 micrograms/l) and sensitivity (lower range less than 1 microgram/l). The assay can be adapted for use on tissue cytosol as well as plasma. Healthy subjects showed plasma lactoferrin levels ranging from 187.5-450.1 micrograms/l. Pulmonary tuberculosis and acute pneumonia are associated with a 2-3-fold increase in plasma lactoferrin content while neutropenic subjects have markedly depressed lactoferrin concentrations. The assay will be useful for further delineation of lactoferrin and neutrophil function and turnover. | |
| 1108177 | Complications of transrectal aspiration biopsy of the prostate. | 1975 | Four cases of coli-sepsis, one with a fatal outcome have been observed after more than 14 000 transrectal aspiration biopsies (TAB) of the prostate performed at Karolinska Sjukhuset with Franzén's apparatus. A few cases of transient febrile reaction and urinary contamination after TAB of the prostate have also been recognised. One of the patients with sepsis and two with febrile reactions belonged to a relatively small group of patients referred from the Department of Rheumatology. These observations prompted the present study. The records of all the patients referred for TAB of the prostate from the Department of Rheumatology were reviewed. Four complications (three patients with febrile reaction and growth of E. coli in the urine and one case of sepsis) were observed after 63 biopsies in 51 patients (6.3%). The patient with sepsis and two other patients with complications belonged to a group of 32 patients with proven rheumatic disease (chronic polyarthritis): 42 biopsies had been performed in this particular group of patients, bringing the incidence of complication to 7.1%. For comparison the records of 294 patients from the Department of Urology submitted to TAB of the prostate were also reviewed. Complications in the form of transient febrile reactions were found in five cases after 508 biopsies (1.0%). In addition, three cases of coli-sepsis not belonging to the above-mentioned groups are briefly described as case reports. Patients with rheumatic disease (chronic polyarthritis) seem to run a higher risk of complications after TAB of the prostate. Sepsis from E. coli is a rare but serious complication which can develop into, often fatal, endotoxin shock. TAB of the prostate should therefore be restricted to cases with clinical suspicion of prostatic malignancy. | |
| 6356882 | Significance of a positive antinuclear antibody test in a pediatric population. | 1983 Nov | Clinical and laboratory findings in 138 children seen during a ten-year period with a positive antinuclear antibody (ANA) test were reviewed. Two thirds (91 of 138) of the patients had specific autoimmune or rheumatic diseases, including systemic lupus erythematosus (n = 37), juvenile rheumatoid arthritis (n = 33), Sjögren's syndrome (n = 9), mixed connective tissue disease (n = 7), dermatomyositis (n = 3), and discoid lupus (n = 2). Another 27 patients had symptoms of autoimmune disease but did not fit criteria for specific disorders. Nine patients with IgA deficiency had a positive ANA test but did not have symptomatic autoimmune disease. Ten children had a positive ANA test in association with infections, mainly viral, and one had leukemia. Because most children with a positive ANA test had readily diagnosable autoimmune disorders, pediatric patients with a positive ANA on repeated testing should undergo clinical and laboratory studies for autoimmune or rheumatic disease. | |
| 6279118 | Antibody to cytomegalovirus in patients with Sjögren's syndrome. As determined by an enzy | 1982 Mar | By use of enzyme-lined immunosorbent assay (ELISA), patients with Sjögren's syndrome were found to have levels of serum IgG antibody to cytomegalovirus twice those of matched control subjects, and IgM antibody levels which were three times as high. It may be relevant that features of cytomegalovirus infection are similar to those of Sjögren's syndrome. | |
| 3857944 | Therapy-related acute myeloid leukemia and myelodysplastic syndrome: a clinical and morpho | 1985 Jun | This study consists of 65 patients (pts) who developed a myelodysplastic syndrome (MDS) (39 pts) or acute myeloid leukemia (AML) (26 pts) following chemotherapy and/or radiotherapy; the interval from the onset of therapy to bone marrow abnormality ranged from 11 to 192 months (median, 58). Thirty-three patients had been previously treated for lymphoproliferative diseases, 29 for carcinoma, and three for a nonneoplastic disorder. Approximately 30% of the cases presenting in the MDS phase evolved to AML in one to 12 months (median, 3.5). The AML in 49% of the cases was not readily classified according to French-American-British (FAB) criteria; the primary difficulty in classification related to the involvement of multiple cell lines. Among the cases that could be classified, all FAB types were represented except for M1; M2 was the most frequent type. Clonal chromosome abnormalities were found in marrow specimens from 22 of 24 (92%) patients studied with G banding; 11 had abnormalities of chromosomes 5 and/or 7. The median survival for all patients was four months with no significant difference between those treated and not treated with antileukemic therapy. The median survival was three months for the patients presenting with AML, six months for the patients with AML following an MDS, and four months for the patients with an MDS that did not evolve to AML. The findings in the present study suggest that there are three stages of therapy-related panmyelosis: (1) pancytopenia with associated myelodysplastic changes, (2) a frank MDS, and (3) overt AML. Many patients will present in the stage of overt AML that differs from de novo AML primarily by the high incidence of trilineage involvement, difficulty in classification, frequent cytogenetic abnormalities, and poor response to antileukemic therapy. The myelodysplastic phase, with or without evolution to acute leukemia, is a highly lethal disease with a median survival comparable to that of the patients who present with AML. | |
| 7045623 | Clinical prospects for liposomes. | 1982 Mar | The use of liposomes has recently been the subject of considerable attention as a promising and versatile approach to drug delivery. Particularly intriguing is the possibility of targeting liposomes to specific areas of the body such as tumors or sites of inflammation or parasitic invasion for either local accumulation or release of associated drugs. This review focuses mainly on recent in vivo work having clinical potential. An extensive discussion of liposome preparation and entrapment of drugs for controlled release in vivo is also included. The stability of liposomes in biological fluids is a major problem. The mode of administration, either intraperitoneal, subcutaneous, local, oral, or respiratory, is closely related to the life of the liposomes in vivo. Following in vivo administration the lifetime of a liposome is critically dependent on its composition, size, and charge. Liposome toxicity appears to be minimal, but should be considered when administering liposomes to patients. Tissues such as the liver, spleen, and lungs, because of macrophage ingestion of liposomes, become potential sites of drug toxicity. The use of liposomes to deliver antiparasitic drugs in the treatment of malaria and leishmaniasis is promoting; so it is the use of surfactant-carrying liposomes in the treatment of respiratory distress syndrome in premature babies. Recent cancer studies utilizing liposomes both in vivo and in vitro have shown promise. In tumor-bearing animals a liposome drug delivery system has caused a regression, delayed tumor growth, and increased survival time. Although the clinical use of liposomes is only in its infancy, its potential in future therapy appears promising. | |
| 6399627 | Primary Sjogren syndrome: clinical and immunopathologic features. | 1984 Nov | Primary Sjogren syndrome is an autoimmune condition in which dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia) result from lymphocytic infiltration of lacrimal and salivary glands. Clinical and laboratory features of 60 primary Sjogren syndrome patients seen at our clinic during the past three years are presented. These patients illustrate the wide spectrum of extraglandular features that may occur as a result of lymphoid infiltration of lung, kidney, skin, stomach, liver, and muscle. They further emphasize the difficulty in classifying a patient as primary or secondary Sjogren syndrome (ie, sicca symptoms associated with systemic lupus erythematosus, rheumatoid arthritis, or scleroderma), particularly early in the disease course. As an initial step in understanding the pathogenesis, the lymphocytes that infiltrate the salivary glands and lymph nodes were characterized by using monoclonal antibodies that recognize distinct lymphocyte subsets and by using in vitro functional assays. These studies have demonstrated that affected tissues have infiltrates of T cells with helper/inducer activity and with a high frequency of "activation antigens." The immunohistologic techniques are useful in differentiating "benign" and "pseudolymphoma" lesions (both due predominantly to T cells) from non-Hodgkin lymphoma (usually due to B-cell infiltrates). Although there is no "cure" for primary Sjogren syndrome patient's symptoms may be significantly improved by measures aimed at prevention of ocular and dental complications and by the recognition of extraglandular features that may be amenable to specific treatment. | |
| 4125373 | Mechanisms of lysosomal enzyme release from human leukocytes. I. Effect of cyclic nucleoti | 1973 Jul | In order to study mechanisms underlying selective enzyme release from human leukocytes during phagocytosis, the effects were studied of compounds which affect microtubule integrity or the accumulation of cyclic nucleotides. Human leukocytes selectively extrude lysosomal enzymes (beta-glucuronidase) from viable cells during phagocytosis of zymosan or immune complexes, or upon encounter with immune complexes dispersed along a non-phagocytosable surface such as a millipore filter. In each circumstance, lysosomal enzyme release was reduced by previous treatment of cells with pharmacological doses of drugs which disrupt microtubules (e.g. 10(-3)-10(-5) M colchicine) or with agents which affect accumulation of adenosine 3'5'-monophosphate (cAMP) (e.g. 10(-3) M cyclic nucleotides and 2.8 x 10(-4)-2.8 x 10(-6) M prostaglandin E (PGE) and A (PGA) compounds). Preincubation of cells with 5 microg/ml cytochalasin B resulted in complete inhibition of zymosan ingestion, but not of adherence of zymosan particles to plasma membranes or selective enzyme release. In this system, in which enzyme release was independent of particle uptake, preincubation of cells with colchicine, vinblastine, dibutyryl cAMP, or PGE(1) also reduced extrusion of lysosomal enzymes. When cell suspensions were incubated with membrane-lytic crystals of monosodium urate (MSU), cytoplasmic as well as lysosomal enzymes were released with subsequent death of the cells. However, enzyme release followed phagocytosis of crystals (as measured by enhanced C-1 oxidation of glucose) and was due to "perforation from within" of the lysosomal membrane, rather than lysis by crystals of the plasma membrane. Enzyme release after MSU ingestion was also reduced when cells were treated with pharmacological doses of the test agents. When cells were killed by Triton X-100, acting on the plasma membrane, C-1 oxidation of glucose was abolished and enzyme release could not be inhibited pharmacologically. These observations suggest that lysosomal enzyme release from human phagocytes can be an active process which accompanies plasma membrane stimulation, is independent of cell death, and may be controlled by cyclic nucleotides and agents which affect microtubules. | |
| 6309959 | Immunoregulatory human T lymphocytes triggered as a consequence of viral infection: clonal | 1983 Sep | The regulatory functions of a series of human T cell clones specific for an autologous Epstein-Barr virus transformed B lymphoblastoid cell line were examined. Two T4+ T cell clones, termed AT4II and AT4IV, and one T8+ clone, AT8III, were maintained in culture for greater than or equal to 9 months and were characterized in detail. Both T4+ clones provided helper function for autologous B cell immunoglobulin production when added to unstimulated peripheral blood mononuclear cells. In addition, these same clones produced soluble inducer factors after specific antigenic stimulation. However, when AT4II, AT4IV and their subclones were tested on pokeweed mitogen stimulated peripheral blood mononuclear cells, it was found that AT4IV provided help for immunoglobulin production whereas AT4II cells were strongly suppressive. This suppression by AT4II was indirect and required the presence of fresh, autologous, unirradiated T8+ cells. In contrast, the T8+ AT8III clone markedly inhibited Ig production by autologous B cells in the absence of any additional T8+ cells from peripheral blood and produced a soluble suppressor factor upon specific antigenic triggering. Thus, after stimulation with autologous Epstein-Barr virus transformed cells, at least three discrete regulatory human T cell populations can be defined at the clonal level: helper, inducer of suppression and suppressor effector clones. | |
| 4111367 | Naturally occurring human antiglobulins with specificity for E. | 1972 Apr | Human sera have been examined for antibodies with specific reactivity for gammaE using the tanned cell hemagglutination test. Cells tanned with three different gammaE myeloma proteins provided a reproducible test system. Inhibition of agglutination reactions by gammaE proteins, but not by gammaG, gammaA, gammaM, or gammaD confirmed the specificity of these reactions. 8.5% of 304 serial serum samples obtained from miscellaneous hospitalized patients showed clear-cut anti-gamma-globulins with specificity for gammaE. In most of these instances no definite clinical history of concomitant allergic disorders could be obtained. 53% of 73 patients with well-established allergic disorders (hay fever, extrinsic asthma) showed serum anti-gamma-globulins with reactivity for gammaE. Some patients studied before and after desensitization to Bermuda grass allergen showed an increase in titer or a conversion from negative to positive reactions for anti-gammaE antibodies following several month courses of progressive desensitization. Gradient and gel filtration studies indicated that anti-gammaE globulins were 19S gammaM in all instances. No clear correlation was noted between quantitative serum gammaE levels and titer of anti-gammaE antibodies.19S serum fractions with anti-gammaE antibody activity did not release histamine from normal human peripheral blood leukocytes, whereas specific rabbit anti-gammaE antisera consistently induced leukocytic histamine release. Moreover, macroglobulin fractions with anti-gammaE activity did not block allergen-specific leukocyte histamine release induced by in vitro leukocyte challenge with allergens such as Bermuda grass and leukocytes from allergic donors. In some instances 19S human serum fractions with anti-gammaE activity appeared to potentiate histamine release when incubated concomitantly with specific allergen and leukocytes from allergic individuals. | |
| 3877510 | Two types of inflammatory vascular disease in Sjögren's syndrome. Differential associatio | 1985 Nov | Two types of inflammatory vascular disease (IVD) occur in Sjögren's syndrome: neutrophilic IVD (NIVD) and mononuclear IVD (MIVD). In 45 patients with Sjögren's syndrome, we examined the 2 types of IVD with respect to serologic associations. NIVD, unlike MIVD, was significantly associated with seroreactivity reflected by hyperglobulinemia (P = 0.01), rheumatoid factor (P = 0.002), antinuclear antibodies (P = 0.02), and antibodies to Ro (SS-A) (P = 0.00006), and with hypocomplementemia (P = 0.03). The differential association of the 2 types of IVD with serologic reactivity and hypocomplementemia suggests that there may be basic differences in the immunopathogenesis of these 2 forms of IVD in Sjögren's syndrome. | |
| 238789 | Calcification of the heart and great vessels. | 1975 Apr | Calcification of the heart and great vessels is secondary to those diseases which cause a significant alteration of tissue matrix. Metabolic derangements can cause microscopic calcification of heart muscle, but this has not been demonstrated conclusively roentgenographically. The deposition of calcium may follow a single event or be the result of a longstanding process. The etiology and roentgen appearance of calcium deposition in the various tissues which comprise the heart and great vessels are reveiwed. The common as well as the rare cases are considered; if possible, each entity is demonstrated roentgenographically. In addition, an attempt is made to reciew various points of view, which at times are conflicting. The prognostic importance of cardiac, aortic, or pulmonary arterial calcification is underscored whenever possible. | |
| 6184190 | Anti-golgi complex autoantibodies in a patient with Sjögren syndrome and lymphoma. | 1982 Sep | During routine immunofluorescence studies of the serum of a patient with Sjögren's syndrome and lymphoma we detected antibodies giving a cytoplasmic pattern which did not correspond to previously described patterns found for autoantibodies. Using different cells and tissues as substrates for indirect immunofluorescence, including rat liver, rat small bowel, rat testicle, human thyroid, guinea-pig plasma cells and cultured human fibroblasts, the cytoplasmic structure to which these autoantibodies are directed seems to be the golgi complex, a conclusion supported by histochemical studies. Furthermore, these antibodies were absorbed by isolated golgi vesicles. The autoantibodies are of IgG and IgA classes, and the antigen(s) with which they react is(are) resistant to treatment with DNAse and RNAse. None of the sera from 50 normal individuals, seven patients with Sjögren's syndrome (five of them primary and two associated with rheumatoid arthritis; none of them with lymphoma), 25 patients with mixed connective tissue disease, 10 patients with systemic lupus erythematosus and five patients with progressive systemic sclerosis, had antibodies directed against this cytoplasmic specificity, as determined by indirect immunofluorescence. This is the first time that autoantibodies directed to the golgi complex are reported. The significance of this finding awaits further descriptions in patients with a clinical picture similar to the one reported here. | |
| 1008618 | Defective responsiveness to ascorbic acid of neutrophil random and chemotactic migration i | 1976 Dec | Polymorphonuclear (PMN) leucocytes from 4 patients with untreated systemic lupus erythematosus (SLE) showed defective random migration (P less than 0-05) and depressed chemotactic responses to C5a and kallikrein (P less than 0-01) compared to PMN leucocytes from normal subjects, or patients with rheumatoid arthritis (4) or Felty's syndrome (4) when examined at a standardized cell concentration with a micropore filter radioassay but not with a conventional Boyden technique. Normal in vitro enhancement of PMN leucocyte random and chemotactic migration by sodium ascorbate was absent in SLE and Felty's syndrome, but sodium ascorbate gave normal stimulation of hexose monophosphate shunt activity in the PMN leucocytes precluding a defect in ascorbate transport. | |
| 6210306 | Inhibition of soluble antigen-induced T cell proliferation by warm-reactive antibodies to | 1984 Dec | One of the fundamental immunologic characteristics of systemic lupus erythematosus (SLE) is a depressed T cell proliferative response to various specific and nonspecific stimuli. Both intrinsic cellular defect(s) and inhibitory influences of humoral factors, e.g., antilymphocyte autoantibodies or immune complexes, have been postulated to underly this functional abnormality. Because patient serum can induce SLE-like T cell dysfunction in normal cells, an extrinsic mechanism is probably responsible, but the nature and site of action of this humoral activity has not been defined. This laboratory recently described a novel antibody specific for activated T cells in SLE, which raised the possibility that suppression of T cell proliferation by SLE serum involved antibodies directed to surface determinants expressed during the process of activation. In experiments to examine this concept further, relatively warm-reactive antibodies to T cell blasts were found to inhibit strongly the well-characterized T cell response to tetanus toxoid. These antibodies were distinct from conventional cold-reactive IgM antibodies to resting T cells, which exhibited little inhibitory activity. Inhibition involved noncytotoxic effects on early activation events at the level of the responding T cell, which markedly reduced the expression of receptors for interleukin 2. Inhibitory effects on antigen-pulsed macrophages or on T cells already committed to proliferate were not demonstrable. Anti-T blast antibodies were characteristic of active SLE and were detected only occasionally in patients with inactive disease or non-SLE rheumatic disorders. Although the exact antigenic specificity was not identified, considerable evidence was obtained against the presence of antibodies to Ia and certain other surface determinants of functional relevance. Our observations concerning the suppressive effects of anti-T blast antibodies in SLE serum on the T cell response to tetanus toxoid should provide new insight into mechanisms of in vivo T cell dysfunction in this and other immunologic disorders. | |
| 7334068 | Primary immunodeficiency syndrome in Japan. I. Overview of a nationwide survey on primary | 1981 Jan | The results of a nationwide survey on primary immunodeficiency syndrome (PIS) in Japan are presented. By the repeated questionnaire method, 497 PIS cases were collected prior to February 1979 with clinical information. Numbers of each type of PIS, age at the time of diagnosis, patient's status at the time of registration, familial incidence of PIS, and development of malignancy, autoimmune diseases, and allergic diseases among all reported patients are presented and discussed. | |
| 6902669 | Immune complexes in Sjögren's syndrome. | 1980 Jul | Sera from 48 patients with Sjögren's syndrome were examined for immune complexes by the Raji cell assay. There was no correlation between levels of immune complexes and the degree of lymphocytic infiltration of the labial salivary glands. Serum complement levels were normal. Five patients were serially followed during the development of pseudolymphoma or malignant lymphoma. Immune complex levels in 4 of the 5 patients were generally unchanged throughout the illness and did not parallel disease activity, rheumatoid factor, or SS-A and SS-B concentrations. Possible roles for immune complexes in Sjögren's syndrome are discussed. | |
| 4586872 | T and B lymphocytes in peripheral blood and tissue lesions in Sjögren's syndrome. | 1974 Jan | Lymphocyte heterogeneity was studied in peripheral blood and salivary gland lesions in 24 patients with Sjögren's syndrome. Peripheral blood B cells, measured by immunofluorescence with specific antiserum to immunoglobulins or by rosette assay with complementcoated erythrocytes, were increased in most patients. Peripheral blood T cells, measured by immunofluorescence with rabbit antiserum to human thymocytes or by rosette assay with sheep erythrocytes, were reduced in eight patients. Three had associated rheumatoid arthritis, two had a generalized lymphoproliferative disorder, and one each had scleroderma, systemic lupus erythematosus, and neuropathy. The salivary gland lymphocytic infiltrates present in labial biopsy specimens were compared in 10 patients using an indirect immunofluorescent method with anti-human T cell serum and a quantitative focus-scoring method. In general, there was a correlation between the number of T cells and the extent of the infiltrate. Striking accumulations of T cells were present in some patients, but clusters of presumed B cells were also seen. These results indicate an increase in peripheral blood B cells in most patients, a decrease in T cells in some, and a mixed T and B cell infiltrate in the salivary gland lesions. | |
| 6196033 | Phenotypic characterization of cells within subcutaneous rheumatoid nodules. | 1983 Nov | An immunohistochemical double-staining technique was applied to frozen sections of biopsies from subcutaneous rheumatoid nodules. Material within the central necrosis reacted with anti-immunoglobulin and anti-HLA-DR antibodies. Cells within the palisading layer were "macrophage-like," as indicated by staining for anti-HLA-DR and OKM1, and showed a high proliferative activity as seen by OKT9 reactivity. The granulation zone contained many (alpha Leu-1+) T cells in close contact with HLA-DR-expressing non-T cells. | |
| 583182 | [Unusual autoimmune and neoplastic associated diseases in Sjogren's syndrome]. | 1979 Nov 24 | In an unselected series of 12 patients with Sjögren's syndrome the following autoimmune diseases were observed: severe myxedema due to Hashimotos thyroiditis in four, subclinical thyroid hypofunction in one, diffuse hyperthyroidism in one, glomerulonephritis in two, chronic active hepatitis in one, lupus erythematodes disseminatus in three (one with idiopathic thrombocytopenic purpura), classical rheumatoid arthritis in two. A rare familial occurrence was seen in two sisters. The only male in this group exhibited coexistence of a benign adenolymphoma of the parotid gland (Warthin's tumor) with a malignant non-Hodgkin lymphoma. |