Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
| ID | PMID | Title | PublicationDate | abstract |
|---|---|---|---|---|
| 6966499 | An epidemiologic study of households exposed to canine systemic lupus erythematosus. | 1980 May | To determine whether exposure to canine lupus is a risk for human lupus, we studied 83 members of 23 households exposed to 19 dogs with high titer antinuclear antibodies and compared these contact households to 50 members of 18 control households matched for dog age, sex, and primary veterinarian. No differences were found between contacts and controls in titer of antinuclear, antiDNA, antiRNA, and antilymphocyte antibodies, frequency of positive rheumatoid factor, or elevated serum immunoglobulins. Further analysis of subgroups by age, sex, and intensity of dog exposure did not reveal any serologic differences between contacts and controls. No cases of lupus were identified in either group. Three contact households and no controls reported a family history (remote from the household) of lupus. This study did not detect any clinical or serologic effect of human household exposure to dogs with high titer antinuclear antibodies. | |
| 4066202 | A new test method for the standardized evaluation of changes in the ultrastructure of chon | 1985 | By means of a new ultrastructural test system, which is based on standardized morphometry and statistical evaluation, we are able for the first time to quantify changes in the cell metabolism of chondrocytes in the articular cartilage. To compare anti-inflammatory substances of different structure, different absorption characteristics and pharmacokinetics as regards their effect on rat cartilage, we used an equieffective dosage of the different anti-inflammatory drugs. Dexamethasone as steroidal and indomethacin and phenylbutazone as classical non-steroidal anti-inflammatory drugs (NSAIDs) were administered in an ED50 dosage referred to provoked arthritis over 12 weeks, using the same mode of administration. The standardized results of untreated rats weighing 300 and 450 g were used as the controls. Dexamethasone brings about massive degenerative changes in the ultrastructure of the vital chondrocyte. Under indomethacin and phenylbutazone the metabolic activity of the chondrocyte is inhibited to a much lesser extent. The damage to the chondrocyte after treatment with dexamethasone, indomethacin and phenylbutazone cannot be regarded as minimal but in some cases is tolerable as regards the benefit/risk ratio in the treatment of rheumatoid diseases. | |
| 6466714 | Degradation of cartilage proteoglycan and collagen by synovial cells. Stimulation by macro | 1984 Aug 17 | When cultured together with dead 35S-labelled cartilage discs or at the surface of [3H]proteoglycan/[14C]collagen-coated plates, synovial cells from either arthritic or normal rabbit joints digested both the proteoglycan and the collagen of the substrates after a lag-period of 1-2 days. These digestions were inversely related to the age (number of subculture passages) of the synovial cells and they could be modulated by serum components that were either inhibitory or stimulatory. They were dependent on a protein synthesis by the cells and were paralleled, in young cultures, by the release of collagenase and of a proteoglycan-degrading neutral proteinase. The co-culture of synovial cells with macrophages or their culture with macrophage-conditioned culture media caused a more rapid and more extensive degradation of collagen and proteoglycan due to the stimulation of the synovial cells by a nondialysable macrophage factor. The production of this synovial cell-activating 'matrix regulatory monokine' by the macrophage was enhanced by several immunological or inflammatory stimuli such as lymphocyte factors, phagocytosis, asbestos fibres, endotoxin, adjuvant muramyl dipeptide or chemotactic formyl-methionyl peptide, as well as by other membrane-active agents (phorbol myristate acetate, concanavalin A). It is presumed that these interactions are of importance in the development of cartilage destruction in rheumatoid and other chronic inflammatory arthritis. | |
| 3159084 | [Analysis of T-cell subpopulations. Pathophysiological concept and significance for clinic | 1985 Apr 20 | Two T-lymphocyte subsets develop in the thymus which differ in the expression of glycoproteins on their cell surface. About 60% of the circulating T cells express the glycoprotein T4, while about 30% have the glycoprotein T8. T4 and T8 cells can be determined in the peripheral blood or various organs with monoclonal antibodies. T4 and T8 cells differ in their antigen recognition, have different functions, and can cause various pathohistological changes. T4 cells recognize the antigen in association with the HLA-D/DR/DP determinants. Upon antigenic stimulation they liberate various factors and initiate and amplify an immune response (T4 = helper/inducer T-cells). They can also be cytotoxic and are mediating effector functions via macrophage activation. T8 cells recognize the antigen in association with HLA-A/B/C determinants. They exert their cytotoxic or suppressive effector functions mainly in viral infections. The T4 or T8 cell-mediated pathohistological changes are discussed in the light of the well studied T-cell infiltrations in lepra lepromatosa or lepra tuberculosa. The T4/T8 cell dyscrasia in the peripheral blood, described in a variety of infectious, autoimmune or immunodeficiency diseases, may be due to enhanced proliferation, selective sequestration, reduced production or the elimination of a subset. T-cell subset analysis in joints, bronchial lavages and tissues has clarified the pathomechanism in a variety of autoimmune diseases, although the etiology remains obscure. For example, in rheumatoid arthritis, multiple sclerosis, and sarcoidosis, a T4 cell-mediated reaction with macrophage activation can be found. T4/T8 cell analysis may also be of value in dissecting heterogenous diseases, e.g. systemic lupus erythematosus. Of value is also the additional demonstration of membrane components reflecting T-cell activation (IL-2 receptor or DR-antigen expression) which serves to identify the activated T-cell subset in peripheral blood. Finally, T4/T8 cell analysis can be helpful in deciding treatment, as the T-cell subsets have a different sensitivity to immunosuppressive drugs. | |
| 6333888 | Chronic T cell lymphocytosis: a review of 21 cases. | 1984 Nov | Twenty-one patients are described with a proliferation of morphologically mature T lymphocytes. The clinical course was chronic in most, and splenic enlargement the main clinical finding; skin involvement and lymphadenopathy were rare. The mean lymphocyte count at presentation was 8 X 10(9)/1 (range 0.75-24 X 10(9)/1). Nineteen of these patients showed some form of cytopenia (18 neutropenia, two red cell aplasia, eight thrombocytopenia) and one had hypogammaglobulinaemia. Seven patients had long-standing arthropathy serologically proven to be rheumatoid arthritis and these had previously been considered to have Felty's syndrome. Five of the group have died (three with an aggressive course), but most have remained stable for prolonged periods with a slow increase in peripheral lymphocyte count and marrow infiltration. Spontaneous regression was never observed but in two patients a prolonged remission was achieved by chemotherapy. The lymphocytes were morphologically and phenotypically homogeneous at presentation and remained so post-splenectomy; they contained azurophilic granules, stained with acid phosphatase but weakly or not at all with alpha napthyl acetate esterase. Membrane phenotyping shows the majority of the cells to be E+, Fc gamma+, OKT3+, OKT8+. Most cells do not stain with OKT1-like reagents and a significant number express HLA-Dr. From these and other reported cases it is clear that this condition represents a distinct entity resulting from the expansion of a subset of cytotoxic/suppressor T cells--the question of the benign or neoplastic nature of the disease remains open. Using T cell-specific antisera and E-rosetting techniques, a small percentage of CLL cases have been shown to be of T-cell origin (TCLL) (Dickler et al, 1973; Lille et al, 1973). Estimates of the percentage vary but in most series T-CLL has been diagnosed in less than 5% (Brouet & Seligmann, 1981), and this is supported by date from the M.R.C. Leukaemia Unit which found T-CLL in only 1.5% of 600 cases of CLL examined by marker studies (D. Catovsky, unpublished). Amongst the published reports of T-CLL a variety of clinical and morphological entities have been described including T prolymphocytic leukaemia (TPLL) (Brouet et al. 1975) and adult T cell disease in Japanese (Uchiyama et al, 1977) and West Indian Caribbean groups (ATLL) (Catovsky et al, 1982). In the original series of Brouet & Seligmann (1981) the group was defined as presenting in middle age with marked hepatosplenomegaly, some lymphadenopathy, skin involvement and with an aggressive disease course; peripheral blood and marrow lymphocytosis were variable.(ABSTRACT TRUNCATED AT 400 WORDS) | |
| 6611368 | Regulation of antibody release by naturally occurring anti-immunoglobulins in cultures of | 1984 Sep | Immunoregulatory influences of human anti-immunoglobulins (anti-Ig) were studied in cultures of peripheral blood lymphocytes (PBL) from 11 normal donors. Pokeweed mitogen (PWM)-stimulated PBL released anti-Ig specific for Fab or Fc fragments of IgG, often within the first 24 to 72 hr in vitro. PBL that released more than 1 ng/ml IgM anti-Fab during the first 72 hr in vitro ultimately produced significantly less antibody (Ab) by the 12th day than PBL that released no detectable IgM anti-Fab during the first 3 days in culture. Adding affinity-purified human anti-Fab to PWM-stimulated PBL also suppressed the later Ab release by these cells. Suppression was polyclonal, affecting IgM anti-Fc, IgM anti-Fab, and IgM anti-tetanus toxoid Ab, and was directly dependent on the quantity of anti-Fab added. Anti-Fab Ab, isolated from single donor sera, were more suppressive, nanogram for nanogram, than were equal quantities of IgG anti-Fab obtained from Cohn Fraction II, when added to autologous donor PBL in vitro. Affinity-purified IgM anti-Fc, from pooled rheumatoid arthritis patient sera, also suppressed Ab release by PWM-stimulated PBL in a dose-dependent manner. These observations suggest that anti-Ig may exert a significant immunoregulatory role in man that can override to some extent the T cell-dependent stimulus for polyclonal B cell activation provided by PWM. | |
| 6085600 | Urinary cancer-related protein EDC1 and serum inter-alpha trypsin inhibitor in breast canc | 1984 | In 1976 we isolated a novel glycoprotein labeled EDC1, Mr 27,500, which is immunologically related to the normal plasma protein inter-alpha trypsin inhibitor (IATI, Mr 160,000) and which is the major component of cancer-associated proteinuria. Urinary excretion of EDC1 (mg/g creatinine) may be classified in four ranges: i) low (less than 15); ii) light (15-30); iii) intermediate (31-45); and iv) heavy (greater than 45). Normal healthy women excrete 8.0 +/- 2.2 mg/g creatinine (average +/- SEM), whereas patients with metastatic breast cancer excrete 98.2 +/- 11.6 mg/g creatinine. Patients with a variety of non-malignant disorders excreted 14.6 +/- 4 mg EDC1/g creatinine, but patients with renal failure, rheumatoid arthritis, and infectious diseases averaged 130.3 +/- 60. Sixty-five to 95 percent of urinary immunoreactive EDC1 in the latter group was of higher molecular weight, perhaps reflecting increased renal clearance of plasma IATI. In patients undergoing excisional biopsy of breast lesions, preoperative EDC1 excretion was 21.5 +/- 3.4 in those whose lesions were benign and 43.1 +/- 7.6 in those whose lesions were malignant. Eight of these latter patients were heavy excretors; EDC1 excretion fell postoperatively in these patients. In normal serum the immunoreactive IATI (IR-IATI) exists in three molecular weight forms 160,000, 120,000 and 58,000. In patients who were heavy excretors of EDC1, the IR-IATI corresponding to Mr 58,000 was absent and total serum IR-IATI was about two-thirds of normal. There was also a negative correlation between serum levels of IATI and urinary EDC1 in these patients. These data suggest that urinary EDC1 may arise as a result of interaction between IATI and tumor-associated proteases. | |
| 6600509 | Familial systemic lupus erythematosus: immunogenetic studies in eight families. | 1983 Jan | Familial SLE provides a unique opportunity to study the relationships of previously associated genetic factors (HLA and complement component deficiencies) to the occurrence of SLE, other immune disorders, and autoantibodies in families. Thus, eight families containing two or more affected members with SLE (n = 22) and their relatives (n = 40) were examined for HLA genotypes, complement components and autoantibodies. Among the 40 non-SLE relatives, 7 (18%) had other immune diseases, including thyroid disease in 2, rheumatoid arthritis in 2, ITP in 2, and Henoch-Schönlein purpura in one. This compared to 4 of the 22 SLE patients (also 18%) of whom 3 had thyroid disease and one PSS. Eleven non-SLE relatives (28%) had ANA, which was in high-titer in 5 (13%). Eleven (28%) had antibodies to ssDNA, and one had a BFP. Only the SLE patients had antidsDNA, Ro(SSA), Sm or nRNP. A heterozygous C2 deficiency (C2D) was found in only one of the seven kindreds studied, and followed an A25, B18 DR7 haplotype. Heterozygous C2D, however, was inherited by only one of three family members with SLE. HLA-DR2 occurred in 36% and DR3 in 36% of SLE patients, which was not significantly different from either non-SLE family members or unrelated local controls. Sib pair analysis of seven sets presented here and seven from two published reports, demonstrated only random distribution with SLE. Similarly, other immune disorders and autoantibodies followed no consistent HLA haplotypes or DR specificities. Interestingly, DR2 and/or DR3 were found in five of the six patients (83%) having anti-ro(SSA) antibodies (p = NS). These data strongly suggest that genetic factors (other than HLA and complement component deficiencies) and/or environmental factors are necessary for the expression of SLE and other immune abnormalities in lupus families. | |
| 6181097 | Proteolysis by neutrophils. Relative importance of cell-substrate contact and oxidative in | 1982 Oct | Polymorphonuclear leukocytes have been implicated in connective tissue injury in a variety of disease processes. To gain insight into mechanisms by which neutrophils might degrade connective tissue macromolecules in the presence of proteinase inhibitors, we have used a model system that allows neutrophils to be held in vitro under physiologic conditions in close proximity to a very proteinase-sensitive substrate, (125)I-labeled fibronectin. We have found: (a) neutrophils spread rapidly on the fibronectin substrate; (b) fibronectin proteolysis by neutrophils is largely attributable to released elastase, and is linearly related to cell number over the range of 2,000 to 30,000 cells per assay; (c) oxidants released from neutrophils stimulated by opsonized zymosan or phorbol myristate acetate do not protect released elastase from inhibition by alpha(1)-proteinase inhibitor or alpha(2)-macroglobulin; (d) neutrophil myeloperoxidase and enzymatically generated superoxide anion render alpha(1)-proteinase inhibitor ineffective against fibronectin proteolysis when neutrophils are added 30 min later; and (e) alpha(1)-proteinase inhibitor and alpha(2)-macroglobulin incompletely inhibit fibronectin proteolysis by neutrophils (79.8+/-6.3 and 73.5+/-12.0%, respectively.) The data suggested that proteolysis due to neutrophils that are in contact with susceptible macromolecules may occur due to partial exclusion of inhibitors from the cell-substrate interface. Although confirming that alpha(1)-proteinase inhibitor is ineffective against neutrophil-derived proteolysis after exposure to oxidants, these studies did not support the hypothesis that oxidants released from stimulated neutrophils enhance activity of proteinases they release in the presence of alpha(1)-proteinase inhibitor. We anticipate that further studies with this test system will be helpful in defining conditions that modulate inflammatory connective tissue injury in diseases such as pulmonary emphysema and rheumatoid arthritis. | |
| 3155770 | The isolation and characterization of the human suppressor inducer T cell subset. | 1985 Mar | Immunization of mice with lower primate lymphoid cells has provided a useful strategy for raising monoclonal antibodies against functionally important surface determinants on human T lymphocytes. We have developed a monoclonal antibody, anti-2H4, which defines functionally unique human T cell subsets. This anti-2H4 antibody was reactive with approximately 42% of unfractionated T cells, 41% of T4+ inducer cells, and was reactive with approximately 54% of T8+ cytotoxic/suppressor population. Anti-2H4 was not reactive with human thymocytes, but reacted with subsets of peripheral blood B cells and null cells. This antibody subdivided peripheral blood T4+ cells into two functionally distinct populations. The T4+2H4+ subset proliferate well to concanavalin A (Con A) stimulation, but poorly to soluble antigen stimulation, and provides poor help to B cells for PWM-induced Ig synthesis. The T4+2H4- subset, in contrast, proliferates poorly upon stimulation with Con A, but well on exposure to soluble antigen, and provides a good helper signal for PWM-induced Ig synthesis. What is, perhaps, most important, the T4+2H4+ subset functions as the inducer of the T8+ suppressor cells. Previous attempts to define the latter subset of cells has relied heavily on the use of specific autoantibodies present in the sera of patients with juvenile rheumatoid arthritis (JRA) and systemic lupus erythematosus (SLE). The present results suggest that anti-2H4 antibody defines the human suppressor induced subset of lymphocyte previously described as T4+JRA+. Last, the results reemphasize the previously documented remarkable structural conservation of certain T cell-specific determinants on lymphocytes of phylogenetically distant primates. | |
| 6604044 | Regulation of RNA polymerase I by phosphorylation and production of anti-RNA polymerase I | 1983 | Relative to resting liver, Morris hepatomas with different growth rates (3924A, 5123D, 7800, and 7777) all had higher (two to eightfold) levels (activity/gm tissue) of RNA polymerase I. Only the most rapidly growing tumor (hepatoma 3924A) showed a substantial increase (fivefold) in RNA polymerase III activity. RNA polymerase II activity/gm tissue in the hepatomas was similar to that in resting liver. The elevation in the hepatoma RNA polymerase I activity resulted from both an increase in the number of transcriptionally active enzyme molecules and an increase in the specific activity of the enzyme as a result of phosphorylation. Phosphorylation of RNA polymerase I from Morris hepatoma 3924A could be catalyzed either by an endogenous protein kinase or by a highly purified preparation of NII protein kinase from the same tumor. Three out of eight polypeptides (Mr 120,000, 65,000, and 25,000) or RNA polymerase I were phosphorylated. Phosphorylation resulted in enhanced RNA synthesis at the level of chain elongation. Another nuclear protein kinase, NI, had no significant effect on RNA polymerase I. The activity and/or amount of the NII protein kinase was significantly reduced in resting liver, which correlated with decreased specific activity of the liver RNA polymerase I. Anti-RNA polymerase I antibodies were found in the sera of patients with rheumatic autoimmune diseases such as systemic lupus erythematosus (SLE), mixed connective tissue disease (MCTD), and rheumatoid arthritis (RA). Sera from these patients were capable of specifically inhibiting RNA polymerase I activity in vitro. Antibodies were produced predominantly against three of the polypeptides--S3 (Mr 65,000), S4 (Mr 42,000), and S5 (Mr 25,000) of RNA polymerase I. The spectrum and proportion of the antibodies against these three subunits differ with each patient and with the type of the autoimmune disease. These observations indicate that (1) the NII kinase can regulate RNA polymerase I activity, (2) protein kinase NII is associated with the polymerase I enzyme complex, and (3) certain polypeptides of this enzyme complex may be the target antigens in rheumatic autoimmune disease. | |
| 6817620 | Effect of in vivo administration of gold sodium thiomalate on rat macrophage function. | 1982 Oct | It has been shown that gold accumulates in macrophages. In vitro studies have also shown that long-term anti-inflammatory and immuno-regulatory effects on these cells may be responsible for the effectiveness of gold in the treatment of rheumatoid arthritis. However, the relevance of this information to the in vivo circumstance is largely untested. In this study, the effect of gold sodium thiomalate (AuTM) on rat alveolar macrophage (AM) lysosomal enzymes, bacterial killing, and metabolic activities associated with phagocytosis were assessed after in vivo administration. The activities of beta-glucuronidase, acid phosphatase, and lysozyme were inhibited 1 day following a single AuTM injection (50 mg/kg, subcutaneous). However, lysozyme returned to normal, while the activities of beta-glucuronidase and acid phosphatase were elevated from 4 to 12 days thereafter. When AuTM was administered weekly for 8 weeks, the activities of acid phosphatase and beta-glucuronidase were elevated throughout, while lysozyme was largely unaffected. The increased lysosomal enzyme activities were not due to contamination of polymorphonuclear leukocytes. These long-term effects of AuTm on enzyme activity were in marked contrast to its in vitro effect which inhibited the activities of beta-glucuronidase and acid phosphatase. No effect of AuTM administration on the release of beta-glucuronidase upon phagocytosis of opsonized zymosan was observed. At 1 day following a single AuTM injection or 3 days after a second weekly injection, in vivo bactericidal activity of AM toward S. aureus was diminished. This bacterial killing defect was not due to decrease phagocytosis; the in vivo binding and ingestion of bacteria were normal. The defect correlated with imparied metabolic activities associated with phagocytosis, namely a significant decrease in the reduction of nitroblue tetrazolium and the stimulation of the hexose monophosphate shunt. This may be an attractive anti-inflammatory effect in light of the destructive potential of the reactive oxygen species produced by macrophages in an arthritic circumstance. | |
| 3878694 | [Neonatal antinuclear antibodies and the lupus syndrome]. | 1985 Aug | Neonatal lupus syndrome can be considered as being associated with pregnancy in women with lupus. Two antinomic cases are reported: a pregnancy in a woman presenting with Sjögren's syndrome, bearing a child with neonatal lupus syndrome (atrioventricular block and antinuclear antibodies) and a pregnancy in a woman presenting with lupus and giving birth to a normal child with antinuclear antibodies. These 2 case reports allow us to speculate on the pathophysiology of neonatal lupus syndromes in which the type of antinuclear antibodies seems to play a major role. | |
| 3856736 | [Lithium in the therapy of hematologic diseases in childhood]. | 1985 Feb | The literature as well as the author's data of this topic are reviewed. Lithium stimulates myelopoesis in vitro, especially via CSF-production. This effect is associated with a modulation of cyclic nucleotides. Lithium stimulates leukemic cell lines too. However, according to epidemiological data lithium does not play an etiological role in leukemia. Furthermore, lithium does not stimulate several tumor cell lines in culture. The effect of cytostatic drugs as well as remission rates are not lessened by lithium. In spite of increased production the functions of the granulocytes are not impaired. Because of the wide range of serum level variation serum level determinations are mandatory. To treat hematological disorders a serum level between 0.7 and 1.2 mmol/l should be achieved. Flame emission photometry and atomic absorption photometry are equivalent methods for determination of the serum level. CNS, thyroid gland, kidney, electrolyte balance, gastrointestinal tract have to be monitored for side effects. Lithium therapy has not be given in pregnancy and to breast feeding mothers. In neutropenia with increased susceptibility to infections lithium therapy including serum level monitoring can be given. Lithium reduces leukopenia and infections following cytotoxic chemotherapy for solid tumors. Current pediatric studies are investigating whether patients with chemotherapy induced neutropenia benefit from this effect in terms of increased and prolonged remission rates. | |
| 7172501 | Polymorphonuclear leucocytes release a factor(s) that induces platelet aggregation and ATP | 1982 Sep | We have found that human polymorphonuclear leucocytes (PMN) can be stimulated by large aggregates (heat-aggregated IgG, chemically polymerized IgG, heavily aggregated human immune complexes) and by surface-bound immune complexes (IC) to release enzymes (lysozyme, beta glucuronidase) and a factor(s) able to induce platelet aggregation and ATP release from the platelets. Surface-bound IC were most effective in stimulating the release of this factor(s). We used several substrates for their preparation: plastic-adsorbed antigen. Sepharose-coupled antigen and polymerized antigen. The platelet-aggregating factor(s) released by IC-stimulated PMN and zymosan-stimulated PMN were compared for their susceptibility to inhibition by indomethacin. Both induced a first phase of platelet aggregation that was resistant to indomethacin, but the second phase of aggregation and the release of platelet ATP were inhibited to a variable degree, more pronounced in the case of the factor(s) released after PMN-IC interaction. The lack of inhibition of the early phases of aggregation induced by our factor(s) when platelets were simultaneously exposed to indomethacin suggests that the classical, phospholipid PAF is released under these experimental conditions. Although, further experiments will be necessary to fully characterize the factor(s) involved, our observations suggest a complex interrelationship between human PMN and platelet activation, which may play an important role in the sequence of events that mediate the tissue deposition of IC and appearance of inflammatory changes. | |
| 7035465 | Nonhistone nuclear antigens reactive with autoantibodies. Immunofluorescence studies on di | 1981 Dec | Sera from patients with certain autoimmune diseases tht contained autoantibodies to nonhistone nuclear antigens were used as reagents in an indirect immunofluorescent study. The distribution of these nuclear antigens was determined in synchronized human B lymphoid cells. Autoantibodies to Sm antigen, nuclear ribonucleoprotein complex and SS-B antigen were used. Although all three nonhistone antigens appeared to show speckled nuclear straining patterns in the Go phase, different patterns of staining were present at other periods of the cell cycle. The SS-B antigen showed a distinctly nucleolar localization during the G1/early S phase. These studies demonstrate that autoantibodies occurring in certain human diseases can be useful reagents for the immunohistological localization of nuclear macromolecules and for tracing their pathways during different phases of cell growth and differentiation. | |
| 6790198 | Low molecular mass IgM in urine of patients with primary and secondary renal diseases. | 1981 Jul 1 | Urine specimens from 50 patients with various renal diseases and from 10 normal subjects were examined for the presence of low molecular mass (7S) IgM by double diffusion, using a specific anti-7S IgM serum. 7S IgM in urine was also quantitated by radial immunodiffusion in 5% polyacrylamide gel. It was found with high frequency in the urine of patients with secondary renal diseases associated with multi-system immunological disorders, especially in systemic lupus erythematosus. Two of the patients with lupus nephritis and positive results for 7S IgM in urine were initially diagnosed as nephrotic syndrome due to a primary renal disease; the symptoms and signs of systemic lupus erythematosus developed later. However, 7S IgM was not detected in the urine of patients with primary renal diseases (except for two cases of nephrotic syndrome), nor in normal subjects. Thus detection of 7S IgM in urine may be helpful in the differential diagnosis of primary and secondary renal diseases. | |
| 1083722 | Antibodies to components of extractable nuclear antigen. Clinical characteristics of patie | 1976 Apr | Forty-four patients with antibodies to ribonuclease-sensitive extractable nuclear antigen (ENA), ribonuclease-resistant ENA, or both, are described. Most patients with antiribonucleoprotein (anti-RNP) antibodies have overlapping features of systemic lupus erythematosus (SLE), progressive systemic sclerosis (PSS), and polymyositis, and have a low incidence of nephritis. Most patients with antibody solely to ribonuclease-insensitive ENA have SLE; these patients with SLE are typical of the general SLE population, except that they demonstrate an increased incidence of Raynaud phenomenon. Furthermore, it is shown that antibody to ENA may occur in other rheumatic and nonrheumatic diseases, and that not all patients who have a clinical overlap of SLE and PSS that is suggestive of mixed connective tissue disease have anti-RNP antibody. | |
| 2417765 | Molecular analysis of the RNA and protein components recognized by anti-La(SS-B) autoantib | 1985 Dec | The aim of this study was to determine whether sera with autoantibodies to the La(SS-B) nuclear antigen react with the same or different sets of cellular or viral ribonucleoproteins (RNPs) and whether patients with anti-La(SS-B) comprised a homogeneous group with respect to phenotypic and serological markers. The 34 anti-La(SS-B) sera studied were detected in the course of screening 2,000 sera referred from patients with suspected or defined multisystem autoimmune disease. Analysis of the molecular components of the small nuclear (sn) RNPs isolated from immune complexes developed in vitro between the IgG fractions of the anti-La(SS-B) sera and cell lines selected for their content of viral and cellular (non-viral) RNA showed that all 34 anti-La(SS-B) sera reacted with the same group of cellular RNAs and with two viral RNAs encoded by Epstein-Barr virus. The La(SS-B) RNPs contained one major 50,000 dalton antigenic polypeptide that resolved into 5-6 heterogeneously charged isospecies on two-dimensional immunoblots. In addition to anti-La(SS-B) reactivity, all 34 sera were shown to contain anti-Ro(SS-A) activity by counterimmunoelectrophoresis (CIEP); however, with three exceptions, the antigenic Ro(SS-A) polypeptide was not detectable by immunoblotting. The homogeneity of this group with anti-La(SS-B) was indicated by the findings that of the 34 cases 31 (88%) had hypergammaglobulinaemia, 33 (97%) had rheumatoid factor and 27 (of 30 tested, 90%) were HLA-B8. Thus all anti-La(SS-B) sera react with the same set of RNAs associated with an antigenic 50,000 dalton nucleoprotein, and the presence of anti-La(SS-B) autoantibodies identified a homogeneous group of patients with the serological and phenotypic features of primary Sjögren's syndrome. | |
| 6980631 | C2 deficient systemic lupus erythematosus: its association with anti-Ro (SSA) antibodies. | 1982 Aug | C2 deficiency is the most common complement component deficiency. While individuals with C2 deficiency may be completely normal, a lupus erythematosus-like disease process has developed in some. A 28-year-old woman had a chronic photodermatitis, arthralgias, and mesangial lupus nephritis, She has C2 deficiency associated with an HLA-Dw2 transplantation antigen. Her serum has shown antibodies to the macromolecule Ro (the A antigen in Sjögren's syndrome), while failing to demonstrate antinuclear antibodies in routine laboratory determinations. |