bluuebunny/crossref_metadata_2025_split huggingface dataset:
Serological monitoring of previously treated lepromatous patients during a course of multiple immunotherapy treatments with heat-killed Mycobacterium leprae and BCG
Authors: DOUGLAS J T , HIRSCH D S , FAJARDO T T , GUlDO L S , KLATSER P R 
Published: July 2010

Summary
Two-hundred and seventy lepromatous patients who had completed treatment received multiple treatments with heat-killed M. leprae and BCG and were monitored for changes in humoral responses to M. leprae-specific antigens. These patients were divided into four treatment groups: placebo (n= 69); BCG (n= 68); M. leprae only (n = 71); and BCG + M. leprae (n= 62). They were monitored for 15 months, receiving five inoculations for each treatment regimen. Two ELISA systems, one measuring antibodies to M. leprae-specific epitopes of the phenolic glycolipid I (NDO-ELISA) and the other of 36-kD protein antigens (INH-ELISA) were used to measure serological changes during this period of immunotherapy. We found no significant increase in serological reactivity with the different treatments, as measured by NDO-ELISA, INH-ELISA similarly showed no significant changes, with the exception of increased values in a small group 13% (36/270) which became skin test-positive during the course of the study. The NDO-ELISA results indicate that use of heat-killed M. leprae or BCG + heat-killed M. leprae did not stimulate the humoral response to the semi-synthetic PG-I antigens of M. leprae. Thus, the NDO-ELISA may be useful in monitoring the outcome of vaccine trials in which killed M. leprae or M. leprae fractions are used, since seroconversion may indicate disease, rather than a response to the vaccine material.
IgG subclasses in human chronic schistosomiasis: over-production of schistosome-specific and non-specific IgG4
Authors: BOCTOR F N , PETER J B 
Published: July 2010

SummaryIgG subclasses were determined quantitatively in sera from 63 Egyptian men who were infected with Schistosoma mansoni. Total and antigen-specific IgG was measured pre- and post-treatment. Total IgG subclass antibodies were determined by immunoradiometric assay (IRMA) using monoclonal antibodies (MoAbs). The anti-worm and anti-egg specific S. mansoni IgG subclass antibodies were quantitatively measured by ELISA using specific MoAbs and standards obtained by affinity chromatography. Our data show that total IgG of the patients was elevated in the range of two to three times above normal. The magnitude of increase differed markedly among the four subclasses of IgG. The IgGl, lgG2 and IgG3 concentrations were approximately two to four times higher than normal, whereas the IgG4 concentration was 20 times normal (9000 mg/l). IgG1 and lgG4 tended to dominate the IgG subclass distribution of anti-soluble worm antigen preparation (SWAP) antibodies followed by IgG2 and lgG3. On the other hand, IgGl and lgG2 dominated the IgG subclass distribution of anti-soluble egg antigen (SEA) antibodies. As with IgGl, IgG2 and lgG3, most IgG4 was non-specific. The role of IgG subclasses in the pathogenesis of schistosomiasis is not clear. However, the high concentration of IgG4 might act as IgE blocking antibody, possibly as anti-idiotypes that may play a role in down-regulation of the immune system when it is challenged with an excess of antigen.
Inhibition of enzyme function by human autoantibodies to an autoantigen pyruvate dehydrogenase E2; different epitope for spontaneous human and induced rabbit autoantibodies
Authors: UIBO R , MACKAY I R , ROWLEY M , HUMPHRIES P , ARMSTRONG J MCD , MCNEILAGE J 
Published: July 2010

SUMMARYAntibodies to the mitochondrial autoantigen M2, characteristic or the autoimmune liver disease primary biliary cirrhosis (PBC), react with the E2 subunit of the pyruvate dehydrogenase enzyme (PDH-E2). We examined the effect of disease sera on the enzyme activation catalysed by the PDH complex. Inhibition of enzyme activity was observed in 19 of 24 sera of patients with PBC with a level of &gt;90% inhibition in 14 at a serum dilution of 1/50. The onset of inhibition by serum was rapid, within the time of mixing, and the inhibitory activity was shown to reside in the immunoglobulin fraction of the serum. The immunoglobulin fraction of control sera from patients with other liver diseases (n= 26) and healthy persons (n= 8) failed to produce inhibitory activity. In addition sera from four rabbits, intensively immunized with a recombinant human M2 autoantigen, gave anti-M2 reactions by fluorescence, ELISA and immunoblotting, but did not inhibit the activity of PDH. The failure of experimentally induced M2 antibodies in rabbits to inhibit is interesting in view of the reactivity of the natural M2 autoantibodies of FBC with the highly conserved site on the enzyme which carries the essential lipoic acid cofactor.
A recombinant topoisomerase I used for autoantibody detection in sera from patients with systemic sclerosis
Authors: VERHEIJEN R , VAN DEN HOOGEN F , BEIJER R , RICHTER A , PENNER E , HABETS W J , VAN VENROOIJ W J 
Published: July 2010

SUMMARY
We report the expression of a cDNA clone encoding 695 carboxyl-terminal amino acids of human DNA topoisomerase I (topoI) in Escherichia coli. More than 96% of the anti-HeLa topoI-positive sera from patients with a connective tissue disease displayed also an immunoreactivity with this recombinant protein (the HTopoA protein). Sera from patients with a definite diagnosis systemic sclerosis and reacting with HeLa topoI, all reacted with the HTopoA protein as well. Sera from patients with systemic sclerosis that did not contain anti-topoI antibodies (about 30% of the systemic sclerosis sera), as concluded from HeLa immunoblot, displayed also no immunoreactivity with our recombinant antigen. By expressing different fragments of HTopoA, we were able to assign at least three different autoimmune epitope regions on the HTopoA protein and we show that over a period of 5 years the amount of anti-topoI antibodies against these regions may fluctutate.
Induction of B cell responsiveness to growth factors by Epstein-Barr virus conversion: comparison of endogenous factors and interleukin-1
Authors: BLAZAR B A , MURPHY A M 
Published: July 2010

SUMMARYImmortalized B lymphocytes produce a factor(s) that stimulates growth of B cell lines carrying Epstein Barr virus (EBV). Stimulatory supernatants derived from B cells also exhibit interleukin-1 (IL-1) activity in costimulator assays with the D10.G4.1 helper T cell line. Experiments with purified macrophage-derived IL-1 and recombinant IL-1β demonstrate that IL-1 stimulates proliferation of the cell lines that respond to the factors from B lymphocyte lines. One B cell line, Ramos, an EBV Burkitt's lymphoma, contrasts with other B cell lines in that it is refractory to the growth enhancing effects of B cell conditioned medium and macrophage-derived IL-1. When EBV was introduced into Ramos cells, growth was enhanced by the factor(s) in B cell conditioned medium (six out of seven lines); growth of EBV-converted Ramos lines (six out of seven lines) also was enhanced by IL-1. These findings demonstrate that infection of a non-responsive transformed B lymphocyte by EBV induces cellular responsiveness to factor-mediated growth stimulation.
Erythrocytes of patients with paroxysmal nocturnal haemoglobinuria acquire resistance to complement attack by purified 20-kD homologous restriction factor
Authors: OKADA N , HARADA R , OKADA H 
Published: July 2010

SUMMARYA 20-kD homologous restriction factor (HRF20) which is a membrane inhibitor of the terminal stage of human complement action can be detected by the monoclonal antibody IF5, and is deficient on abnormal erythrocytes as well as leucocytes from patients with paroxysmal nocturnal haemoglobinuria (PNH). The erythrocytes of PNH patients significantly improved their resistance to homologous complement after adsorption of purified HRF20.
Characterization of the common acute lymphoblastic leukaemia antigen (CD10) as an activation molecule on mature human B cells
Authors: KIYOKAWA N , KOKAI Y , ISHIMOTO K , FUJITA H , FUJIMOTO J , HATA J-I 
Published: July 2010

SUMMARYDistinct expression pattern of CD10 molecules during B cell activation was analysed using in vivo and in vitro systems. By two-colour flowcytometrical analysis, CD10 was found to be expressed at a specificstage of in vivo activating B cells. The expression of CD10 during B cell activation appeared to be unique from that of other activation-related B cell antigens including L29, MA6, OKT9 and OKT10. Although the expression of CD10 was associated with that of the activation-related B cell antigens, CD 10+ B cells could be separated in the distinct fractions to those expressing other activation-related B cell antigens when fractionated by cell gravity. In particular, certain CD10+ B cells were detected positive for the resting B cell antigen, L30. In vitro studies revealed that CD10+ B cells arose from CD10- B cells at an early step of B cell activation, and disappeared lately when activated by Staphylococcus aureus Cowan I. Collectively, CD10 was an antigen transiently expressed at an early phase of B cell activation process. Expression of CD10 and other antigens on Burkitt's lymphomas (15 cases) was studied next. All cases were CD10+, and 87% (13 cases) were also L30+. In addition, six of CD10+ L30+ cases were L29+. This observation suggested that Burkitt's lymphomas were phenotypically similar to the B cells at an early phase of activation, those expressing CD10 and L30, simultaneously. The present study has dissected a precise expression pattern of CD10 on mature B cell activation in vitro and in vivo, and could be implicated for the histogenesis of one of the poorly characterized B cell lymphoma, namely Burkitt's lymphoma.
HLA-DQ-controlled T cell response to soluble egg antigen ofSchistosoina japonicuinin huinans
Authors: OHTA N , EDAHIRO T , ISHII A , YASUKAWA M , HOSAKA Y 
Published: July 2010

SUMMARYWe analysed regulatory inechanisins of the huinan T celt response lo soluble egg antigen (SEA) of Schistosoina japonicuin in vitro. SEA is a crude antigen inixture containing nuinerous cpitopes. We obtained SEA-induced T cell lines froin five patients with chronic schistosomiasis japomca, and tested their proliferative response to molecular weight fractions of SEA. Although all T cell lines showed strong responses to crude SEA, there was a heterogeneity in fraclion-driven responsiveness. All but one T cell line tested failed to respond to SEA fraction I (inol. wt&gt; 18 kD). One patient who was typed as HLA-DQwl/w4, did not show proliferation of CD4’T cells lo fraction I; however, a fraction I-driven helper T cell response was observed when we added HU-11 monoclonal antibody specific for HLA-DQwl/w4. This indicated that the patient had helper T cells to the fraction even though their response was suppressed. Because HLA-DQ had an effect on functional expression of suppressor T cells, i t was suggested that there was epitope-specific regulation of the T cell response to SEA, and HLA-DQ-controlled immune suppression inight be involved in the regulatory systein in huinan chronic schistosome infection.
The effect of the immunomodulator agent AS101 on interleukin-2 production in systemic lupus erythematosus (SLE) induced in mice by a pathogenic anti-DNA antibody
Authors: BLANK M , SREDNI B , ALBECK M , MOZES E , SHOENFELD Y 
Published: July 2010

SUMMARYThe role of the synthetic immunomodulator AS101 on the production of interleukin-2 (IL-2) by spleen cells of mice with SLE was investigated BALB/c female mice, in which SLE was induced by immunization with the pathogenic idiotype of anti-DNA antibody 16/6 IJ were treated with AS101 for 7 weeks 2 and 4 months after induction of the disease. The ability of the splenocytes of the mice with SLE to produce IL-2 was restored after administration of AS101. This effect was particularly impressive when the 7-week AS101 treatment was initiated 4 months after immunization. Despite its beneficial effect on IL-2 production. AS101 exerted no influence on the titres of autoatibodies in the sera of the mice. It also had no effect on clinical parameters of SLE, such as the increased sedimentation rate, proteinuria and low white blood cell counts. Our data indicated that defective IL-2 production in ALE is probably secondary to other disease processes and is not necessarily associated with the production of autoantibodies in this disorder.
Autoimmunity to a 28–30 kD cell membrane DNA binding protein: occurrence in selected sera from patients with SLE and mixed connective tissue disease (MCTD)
Authors: BENNETT R M , CORNELL K A , MERRITT M J , BAKKE A C , HSU P H , HEFENEIDER S H 
Published: July 2010

SUMMARYPrevious experiments have established the presence of a 30-kD DNA binding protein on the surface of human leukocytes. Herein we report that selected sera from patients with systemic lupus erythematosus (SLE) and MCTD are reactive with a 28–30 kD protein on immunoblots of peripheral blood mononuclear cells (PBMC) cell membrane preparations; the reactivity is abolished by prior incubation of the blot with DNA. Antibodies ctuted from the 28–30 kD strip inhibited the binding of 3H.DNA to human PBMC. An immunomatrix of 28–30 kD reactive immunogtobulins was able to extract a 29-kD DNA binding protein from a PBMC cell membrane preparation. Flow cytometry experiments confirmed the cell surface IgG reactivity of sera with T lymphocytes. Additional experiments indicated that cell surface IgG binding was not due to antibodies binding to cell surface DNA, DNA anti-DNA immune complexes reacting with a DNA binding protein, anti-histone antibodies or anti-Sm antibodies. It is hypothesized that this autoimmune response could be one component of an idiotypic network involving anti-DNA antibodies.
Ciprofloxacin enhances T cell function by modulating interleukin activities
Authors: STÜNKEL K G E , HEWLETT G , ZEILER H J 
Published: July 2010

SUMMARY
Ciprofloxacin (CIP) is a quinolone carboxylic acid derivative with a broad spectrum of antibacterial activity. CIP (0.1–30 μg/ml) enhanced DNA synthesis of mouse spleen cells and human peripheral blood lymphocytes (PBL) that had been activated with T cell mitogens or with alloantigens. In addition, CIP increased the amount of IL-2 found in the supernatants of phytohaemagglutinin (PHA)-stimulated human PBL. The presence of CIP in the medium (0.3–10 μg/ml) increased the levels of IL-1 found in the culture supernatants of adherence-enriched mouse macrophages, human monocyte/macrophages and a human monocytic cell line stimulated with lipopolysaccharide. In contrast there was no effect of CIP on the release of IL-1 by freshly isolated human monocytes or by cells of the keratinocyte line, A431. CIP alone had no influence on the basal release of IL-2 by NOB-1 cells, a Tcell line that responds to IL-1 with an increase in IL-2 synthesis, but, in combination with recombinant IL-1, CIP significantly enhanced the release of IL-2 by these cells. The results of this study suggest that CIP modulates the immune response at two levels—the production of IL-2 by activated T cells and the production of IL-1 by activated monocyte/macrophages. However. CIP did not affect the primary antibody response in vitro or in vivo against sheep erythrocytes and ovalbumin respectively. Thus the enhancing action of ciprofloxacin on the immune system appears to be restricted to T cell function and macrophage/T cell interactions.
Inhibition of immune reactionsin vivoby liposome associated transforming growth factor (TGF) type β1
Authors: STRASSMANN G , BERTOUNI D R , EIDELMAN O 
Published: July 2010

SUMMARYIn view of its potent inhibitory capacity on immune cells in culture, we wished to determine the ability of transforming growth factor (TGF) β1 to down-regulate immune responses in vivo. Preliminary experiments suggested that, at the doses used, systemic injection of soluble TGFβ1 could not affect bacterial-induced spleen enlargement in mice. Therefore, we sought to utilize a physiochemical properly of this molecule, namely its high pI, to determine possible association between the ligand and preformed liposomes possessing an opposite charge. TGFβ1 was preferentially associated with negatively charged, but not with neutral, liposomes. These TGHβ1 associated liposomes were able to deliver a suppressive signal to indicator cells in vino. Intravenous injection of TGFβ1, associated with liposomes possessing an opposite charge, into mice immunized with heat-killed Corynobacterium parvum significantly reduced the size of the spleen as well as the number of splcnocytes. Systemically administered TGFβ1 associated liposomes could also inhibit delayed type hypersensitivity reactions to Listeria monocytogenes. These data suggest that appropriately administered, TGFβ1 can inhibit immune responses in vivo.
Inter-mouse strain differences in thein vivoanti-CD3 induced cytokine release
Authors: FERRAN C , DY M , SHEEHAN K , MERITE S , SCHREIBER R , LANDAIS P , GRAU G , BLUESTONE J , BACH J-F , CHATENOUD L 
Published: July 2010

SUMMARYTriggering of the CD3 molecule by in vivo injection of the hamster anti-murine CD3 monoclonal antibody 145-2C11 in adult BALB/c mice leads to massive although transient T cell activation. High levels of tumour necrosis factor (TNF), interferon-gamma (IFN-γ), IL-2, IL-3 and IL-6 are released into the circulation 1 to 8 h after a single 10 μg 145-2C11 i.v. injection. This release induces an impressive self-limited physical reaction associating hypothermia, hypomotility (as assessed by actimetry), diarrhoea, piloerection and even death when high doses (a single dose of &gt; 100 μg/mouse injection) are administered. In vivo injection of 145-2C11 to other selected mouse strains, namely NZW, CBA/J and C3H/HeJ, induced both different cytokine release patterns and sickness. 145-2C11 induced significant release of TNF and IL-2 in all four strains. At variance. IFN-γ was only detected in BALB/c mice sera which, in terms of physical reaction (hypothermia and hypomotility) were the most affected. Higher and long-lasting circulating 1L-3/GM-CSF levels were present in CBA/J sera, correlating with a later recovery. These results underline heterogeneity in the in vivo cell activation pattern among different mouse strains, when triggering T lymphocytes via the CD3/Ti molecule as compared to exclusive targeting of monocyte/macrophages by means of lipopolysaccharide.
Immunogenicity of surfactant. I. Human alveolar surfactant
Authors: STRAYER D S , HALLMAN M , MERRITT T A 
Published: July 2010

SUMMARY
The immunogenicity of lung surfactant derived from amniotic fluid has been well established. We have set out to examine the antigenic similarity of human surfactant to non-human alveolar surfactants currently being used therapeutically in clinical trials with neonatal respiratory distress syndrome. To this end, we raised a scries of eight monoclonal antibodies in rats directed to human surfactant (H1 to H8). All antibodies bound human surfactant as measured by ELISA. Four of these monoclonal antibodies bound surfactant components by Western blot analysis: all bound a 9–10-kD species. In addition, one antibody (H2) bound a protein of 16 kD, one (H8) a 6-kD protein, and one (H6) a 30-kD protein. When mixed with surfactant, three antibodies, H4, H7 and H8, profoundly altered surfactant activity in vitro in the pulsating bubble surfactometer. Three other antibodies, H1, H2, and H5 moderately inhibited surfactant's surface activity. We also examined the cross-reactivity of these monoclonal antibodies with bovine (CLSE) and porcine (Curosurf) surfactants. By Western blot analysis, only H6 bound these heterologous surfactants. Other antibodies did so by ELISA. However, functional assays indicated that antibodies H7, H8 and H4 all greatly inhibited CLSE surface activity in vitro. Five antibodies (H1-H4 and H8) inhibited Curosurf function. Thus, human surfactant species, especially low molecular weight species, are highly antigenic. Antibodies to alveolar surfactants may inhibit surfactant function in vitro. As indicated by Western blot and cross-inhibition data, human lower molecular weight surfactants share epitopes with proteins from therapeutically important porcine and bovine surfactants. The potential importance of these findings to treatment of neonatal respiratory distress syndrome with heterologous surfactants is discussed.
Lack of binding between cryoimmunoglobulins, immunoglobulins and fibronectin: implications for immune complex vasculitis
Authors: BRANDAU D T , O'DONNELL R , KIMMEL-TRUITT V L 
Published: July 2010

SUMMARY
Immunc-complex-mcdiated vasculitis is a frequent complication of rheumatoid arthritis and systemic lupus erythematosus. The mechanism of deposition of immune complexes within the vessel wall in these diseases remains unknown, but probably involves other proteins. Fibronectin is a likely candidate since it possesses the ability to bind to collagen, endothelial cells, and possibly immunoglobulins and immune complexes. In this study, the hinding of libronectin to IgG and IgM cryoglobulins, cold soluble IgM, IgG, IgG subclasses and IgG fragments was investigated in the solution phase. Static light scattering, fluorescence anisotropy. fluorescence intensity, and PEG precipitation studies were used to investigate binding under different conditions of temperature and ionic strength. These studies failed to demonstrate significant binding between fibronectin and IgM, IgG, IgG subclasses and IgG fragments under the conditions studied These findings argue against solution phase binding of fibronectin and immunoglobulins contributing to immune complex vasculitis. The possibility of important surface interactions between these proteins has not been ruled out.
Spatial correlation between thyroid epithelial cells expressing class II MHC molecules and interferon-gamma-containing lymphocytes in human thyroid autoimmune disease
Authors: HAMILTON F , BLACK M , FARQUHARSON M A , STEWART C , FOULIS A K 
Published: July 2010

SUMMARY
In this immunohistochemical study we addressed the question whether aberrant class II MHC expression by thyroid epithelial cells (thyrocytes) in established thyroid autoimmune disease is the result of release of interferon-gamma(IFN-γ) by adjacent lymphocytes. Thyroids from eight cases of Hashimoto's thyroiditis, 13 cases of Graves' disease and 10 cases of focal thyroiditis were studied. Both thyrocytes expressing class II MHC and lymphocytes containing immunoreactivc IFN-γ were found in all 31 autoimmune thyroids. In a serial section study of these thyroids. IFN-γ-exprcssing lymphocytes were found within 50 μ of class II MHC-positive thyrocytes in 89% of 282 randomly selected fields. Conversely, class II MHC-positive thyrocyles were found wilhin 50 μ of aggregates of IFN-γ-positive lymphocytes in 82% of 272 randomly selected fields. These findings support the view that in established thyroid autoimmune disease expression of class II MHC by thyrocytcs is the result of local release of IFN-γ.