bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of a recombinant HIV gpl60 vaccine on monokine production
Authors: DOOLEY D P , COX R A , LOONEY D J 
Published: July 2010

SUMMARYAn investigation was undertaken to determine whether a recombinant gp 160 envelope protein, which is currently being evaluated as a vaccine for AIDS, induces or modulates the production of tumour necrosis factor-alpha (TNF-α) or interleukin-1β (IL-1β). Incubation of monocytes from healthy, HIV-seronegative persons with 0.0001–1.0 μg of the recombinant vaccine did not result in the secretion of TNF-α or IL-1β, nor did the recombinant product augment or suppress monokine production by lipopolysaccharide (LPS) stimulated monocytes. The vaccine was also without a stimulatory or modulatory effect upon TNF-α or IL-1β secretion by monocytes from a patient with the AIDS-related complex (ARC) and from the monocytic THP-1 cell line. The lack of effect of gp 160 on monokine production has important implications for its efficacy as a vaccine for AIDS.
Individual germinal centres of myasthenia gravis human thymuses contain polyclonal activated B cells that express all the VH and VK families
Authors: GUIGOU V , EMILIE D , BERRIH-AKNIN S , FUMOUX F , FOUGEREAU M , SCHIFF C 
Published: July 2010

SUMMARYUsing in situ hybridization, we analysed the immunoglobulin repertoire expressed by the B cells present in myasthenia gravis thymuses from four patients. B cells, mostly in activated state, were clustered in germinal centres, in which multiple isotypes were identified. A majority of cells expressed IgG as compared with IgM. with a roughly similar contribution of k and δ chains. Hybridization with the six VH and the 4 Vk human family probes was observed in serial sections, providing additional evidence that individual germinal centres were polyclonal. The thymic B cell repertoire closely reflected the VH and the Vk family usage of normal peripheral blood lymphocytes with the preferential utilization of VH3, Vk1 and Vk3.
LDL-mediated interaction of DNA and DNA-anti-DNA immune complexes with cell surface
Authors: KABAKOV A E , SAENKO V A , POVERENNY A M 
Published: July 2010

SUMMARYThe effect of low-density lipoprotein (LDL) on the binding of DNA and DNA-anti-DNA immune complexes to cultured human skin fibroblasts was examined. Using radioisotope analysis. ELISA and indirect immunofluorescent staining, a correlation between plasma membrane-bound DNA or DNA-anti-DNA immune complexes and cell-associated LDL was established. It was demonstrated that cytotoxicity and internalization of DNA-anti-DNA immune complexes may be LDL mediated. The data obtained suggest that the binding of the major part of DNA and immune complexes bound to surface of normal skin fibroblasts is due to the formation of a DNA-LDL-LDL receptor linkage. A possible role of LDL-containing immune complexes in the pathogenesis of systemic lupus erythematosus is discussed.
Expression of decay-accelerating factor is reduced on hyperplastic synovial lining cells in rheumatoid synovitis
Authors: ITOH J , NOSE M , FUJITA T , KATO M , OHYAMA A , KYOGOKU M 
Published: July 2010

SUMMARYDecay-accelerating factor (DAF), a membrane inhibitor of homologous complement activation, is present in synovial cells lining joint space and detected in synovial fluid. DAF is considered to protect synovial membrane from complement-mediated injury associated with articular inflammation. We studied the immunohistopathological features of DAF molecules in synovial membrane of rheumatoid synovitis using a DAF-specific monoclonal antibody, IC6. Reacting molecules with the 1C6 antibodies in synovial tissue extracts formed a 70-kD band in Western blot analysis. DAF was strongly detected on the flat synovial lining cells, but weakly on the hyperplastic and multi-layered lining cells in rheumatoid synovitis. The latter cells reacted with anti-Lcu-M3 antibodies specific for a cell surface marker of activated macrophages, sometimes accompanied by C3 and IgM deposition on the superficial synovial membrane. These results suggest that active rheumatoid synovitis characteristically with hyperplastic synovial lining cells is out of control by DAF, thereby permitting further complement-mediated injury.
Human hybridomas derived from CDS+ B lymphocytes of patients with chronic lymphocytic leukemia (B-CLL) produce multi-specific natural IgM (kappa) antibodies
Authors: JAHN S , SCHWAB J , HANSEN A , HEIDER H , SCHROEDER C , LUKOWSKY A , ACHTMAN M , MATTHES H , KIESSIG S T , VOLK H D , KRUEGER D H , VON BAEHR R 
Published: July 2010

SUMMARYGreat numbers of CD5+ B lymphocytes were detected in the peripheral blood of patients with B-CLL. To study the antibody repertoire of this immune cell subpopulation on a monoclonal level, we fused the lymphocytes derived from five different donors to a highly efficient HAT-sensitive heteromye-loma line (CB-F7). A fusion frequency of up to 10-5 allowed us to analyse hundreds of initial hybridoma lines per fusion. In all culture supernatants in three out of five fusions IgM lambda antibodies were detected, in two experiments only IgM kappa was measured, suggesting monoclonality of the primary hybridoma cell lines. The later fusions resulted in hybridomas producing multi-specific antibodies against both an autoantigen and an infectious agent: (i) dsDNA/influenza virus haemagglutinin; (ii) dsDNA/class V outer membrane protein type C from Neisseria meningitidis. However, no antibodies of the described specificity were detected in blood sera of patients, indicating a ‘switch-on’ of the immunoglobulin secretion capacity of malignant B cells during fusion to a myeloma partner. We discuss the results as further evidence for the natural multi-reactive antibody repertoire of CD5+ B cells.
Expression of the neural cell adhesion molecule (CD56) by human myeloma cells
Authors: DRACH J , GATTRINGER C , HUBER H 
Published: July 2010

SUMMARYRecent studies in multiple myeloma indicate that molecules associated with different haematopoietic lineages may be expressed aberrantly by myeloma cells. In order to investigate this phenomenon further, we studied the immunophenotype of bone marrow cells from 21 patients with multiple myeloma using a panel of monoclonal antibodies against T.B. myelomonocytic, and natural killer (NK)-cell antigens. Leu-19/NK.H1 (CD56), a molecule identical to N-CAM, which is normally expressed by neuroectodermal and NK cells, was found in 13 patients (62%). Dual-parameter flow cytometry was used to correlate N-CAM positivity with DNA aneuploidy or cytoplasmic immunoglobuiin expression as markers of myeloma cells. When N-CAM was found positive, other haematopoietic antigens were expressed only in three out of 13 cases (23%). In contrast, myeloma cells not expressing N-CAM frequently exhibited pre-B cell markers, myeloid antigen, and HLA-DR, respectively (seven out of eight cases, 88%). Six out of eight N-CAM-negative myelomas were of the IgG lamba isotype, otherwise no clearcut association with basic clinical and laboratory parameters was noted. We conclude that N-CAM expression is a common finding in multiple myeloma. Whether its expression and the observed antigenic heterogeneity is just a manifestation of malignancy or N-CAM may play a role in the biology of multiple myeloma regarding tumour cell spread, remains to be explained.
Differential control of mesangial cell proliferation by interferon-gamma
Authors: KAKIZAKI Y , KRAFT N , ATKINS R C 
Published: July 2010

SUMMARYRat mesangial cells were shown to be sensitive to recombinant interferon-gamma (IFN-γ). IFN-γ reduced thymidine uptake by these cells and inhibited cell proliferation. Incubation of the cells with 1000 U/ml IFN-μ decreased thymidine uptake by up to 64% and cell numbers were decreased by 17%. The effects of IFN-y were dose and time dependent and were partially reversible by the anti-IFN-γ monoclonal antibody DB-I. This lymphokine did not reduce incorporation of RNA and protein precursors however. Measurements of 3H-uridine and 3H-leucine incorporation indicated significant increases in RNA and protein synthesis (37% and 45%, respectively) on a per cell basis. The mitogenic effects of IL-1 and platelet-derived growth factor (PDGF) were also susceptible to IFN-γ-mediated inhibition but the mitogenic response to epidermal growth factor (EGF) was much less sensitive. Weconclude that while IFN-γ may act to modulate the mitogenic signals provided by some factors such as IL-1 and PDGF, the response to EGF appears to be unaffected.
The gene corresponding to the putative Goodpasture antigen is present in Alport’s syndrome
Authors: SAVIGE J A 
Published: July 2010

SUMMARY
Alport’s syndrome is a heterogeneous group of inherited abnormalities of basement membranes that may result in progressive renal failure, defective hearing and lens abnormalities. The glomerular basement membrane (GBM) characteristically has areas of reduplication, lamellation and attenuation on electron microscopic examination. In the majority of affected males and some females, there is reduced or variable binding of serum from patients with anti-GBM disease (Goodpasture’s syndrome) to these basement membranes. These sera contain antibodies directed against the Goodpasture antigen which has been thought to be located in the non-collagenous domain of the alpha3 chain of type IV collagen and is presumed to be important in cross-linking of the collagen molecules. The reduced staining for the Goodpasture antigen suggests that this structure is either absent or masked in Alport’s syndrome. We have tested DNA from six unrelated individuals with Alport’s syndrome. All had been transplanted for renal failure. The diagnosis of Alport’s syndrome was made on the characteristic electron microscopic appearance of the renal basement membranes (n= 4), the presence of sensori-neural deafness (n=4), a family history of Alport’s syndrome (n=5) and the presence of circulating inhibitable anti-GBM antibody activity post-transplant (n=2), Oligonucleotides (20mers) corresponding to the 5′ and _3′ ends of the known 25 amino acid sequence for the putative Goodpasture antigen were used as primers for amplification of genomic DNA. The products were then blotted and probed with an intermediate 19-mer DNA. All Alport’s patients contained a 75-bp fragment corresponding to the published peptide sequence for the non-collagenous domain of the alpha3 chain of type IV collagen, suggesting that a large deletion of this region, the putative Goodpasture antigen, is unlikely to account for the defect in Alport’s syndrome.
Polymorphism of insulin antibodies in six patients with insulin-immune hypoglycaemic syndrome
Authors: DOZIO N , SODOYEZ-GOFFAUX F , KOCH M , ZIEGLER B , SODOYEZ J C 
Published: July 2010

SUMMARYInsulin antibodies in six patients with immune hypoglycaemic syndrome were studied. The antibodies displayed a higher affinity for bovine insulin in two patients, were specific for human insulin in one patient and non-species specific in the other three patients. The predominant IgG subclass of the insulin antibodies was IgG4 in two patients, IgG3 in two and IgG 1 in two. In one of these, the other three subclasses were also detectable. Insulin autoantibodies of four patients were homogeneous with regard to light chains (k), and those of the other two contained both k and γ light chains. Analysis of insulin immune complex size by fast protein liquid chromatography was possible in three patients and demonstrated immune complexes with elution profile close to that of IgG, although not exactly superimposable to the one obtained with a mouse monoclonal insulin antibody. In two patients, avidity was too low to permit chromatography of the immune complexes, and, moreover, in these two cases insulin antibodies were of the IgG3 isotype and spontaneously formed aggregates independently of insulin binding. We conclude that insulin antibodies of the insulin immune syndrome are polymorphic but different from those generated by insulin therapy.
Ciprofloxacin treatmentin vivoincreases theex vivocapacity of lipopolysaccharide-stimulated human monocytes to produce IL-1, IL-6 and tumour necrosis factor-alpha
Authors: BAILLY S , FAY M , FERRUA B , GOUGEROT-POCIDALO M A 
Published: July 2010

SUMMARYBecause in vitro treatment with quinolones, at pharmacological concentrations, modifies lipopolysac-charide (LPS) induced production of cytokines by monocytes, we studied the effect of orally administered ciprofloxacin (25 mg/kg) on the capacity of peripheral blood monocyles of healthy volunteers to produce tumour necrosis factor-alpha (TNF-α), IL-1 activity, IL-1 a, IL-1β and IL-6 ex vivoin response to endotoxin stimulation. After 7 days of ciprofloxacin, the extracellular and cellular production of TNF-α, the cellular production of IL-1 activity, the extracellular and cellular production of IL-1α, and the cellular production of IL-6 increased significantly. Seven days after the end of the treatment, values returned to basal levels or even lower. To our knowledge, this is the first demonstration that ciprofloxacin can modulate in vivo the capacity of human monocytes to react to an inflammatory stimulus such as endotoxin.
An approach to isolating T cell lines that react to antigens presented on the surface of dendritic cells
Authors: PANCHOLI P , STEINMAN R M , BHARDWAJ N 
Published: July 2010

SUMMARYWe describe an approach that might be useful for identifying antigens on surfaces of antigen presenting cells. It is known that dendritic cells carry antigens in situ and are efficient at clustering antigen-specific T cells. Using the human mixed lymphocyte reaction (MLR) system, we have shown that alloreactive CD4+ T cells can be selected by their capacity to cluster with dendritic cells in the first 2 days of the MLR. Small numbers of clustered cells, 1–10/culture well, could then be expanded as antigen-specific lines in presence of either antigen or mitogen, sodium periodate. Few antigen-specific lines could be isolated from the nonclustered fraction. When T cell lines derived from the dendritic T cell clusters were maintained without antigen, i.e. using second party (syngeneic antigen-presenting cells (APC)) or irrelevant antigen bearing APC, i.e. third-party (HLA-mismatched) stimulator cells plus mitogen, the T cells retained their specificity for the original stimulating alloantigen over the time course tested, several weeks to months. These findings show that by using dendritic cells as immunoadsorbents one can prepare antigen-specific cell lines and maintain the specificity of the lines without the need for adding exogeneous antigen during either immunoselection or cloning. We discuss the possible use of dendritic cells as a means for raising T cell lines and clones that recognize antigens being carried by APC and which might be pertinent to protective immunity and autoimmunity.
Humoral autoimmune response to ribosomal P proteins in chronic Chagas heart disease
Authors: LEVITUS G , HONTEBEYRIE-JOSKOWICZ M , VAN REGENMORTEL M H V , LEVIN M J 
Published: July 2010

SUMMARYThe C terminal region of a Trypanosoma cruzi ribosomal P protein, encoded by the λgtll JL5 recombinant, defined a major antigenic determinant in chronic Chagas heart disease. Immunopurified anti-JL5 antibodies were tested for anti-human ribosome reactivity by immunoblotting. They recognized the parasite ribosomal P proteins and clearly reacted with the corresponding human P proteins. The peptide R-13, that comprises the 13 C terminal residues of the JL5 recombinant and defines the specificity shared between chronic Chagas heart disease anti-JL5 antibodies and the systemic lupus erythematosus (SLE) anti-P antibodies, was used to study the specificity and the IgG subclass distribution of the anti-R-13 response by ELISA. The R-13 autoepitope is recognized mainly by sera from chagasic patients, but not by sera from malaria patients. Moreover, there was a significant correlation between anti-R-13 antibody levels and anti-T. cruzi antibody titres. The anti-R-13 response was mainly restricted to the IgG1 heavy chain isotype and correlated with the anti-T. cruzi isotype distribution.
Increased luminol-enhanced chemiluminescence of blood monocytes and granulocytes in Hodgkin’s disease
Authors: TULLGREN O , GISCOMBE R , HOLM G , JOHANSSON B , MELLSTEDT H , BJÖRKHOLM M 
Published: July 2010

SUMMARYThe oxidative metabolic burst of blood monocytes and polymorphonuclear leukocytes (PMN) from 22 untreated patients with Hodgkin’s disease (HD) and 18 healthy subjects were studied. Monocytes and PMN were enriched by density centrifugation and in vitro activated by zymosan. The oxidative metabolism was measured by luminol-enhanced chemiluminescence (CL). The CL of the patients’ monocytes and PMN was higher than that of controls (P&lt; 0.01 and P± 0.05, respectively). Patients with stage II-IV HD showed an increased blood monocyte CL as compared with stage I patients (P&lt;0.05). Furthermore, patients with lymphocytic depletion or mixed cellularity subtype demonstrated an increased CL of PMN as compared with the remainder. Enhanced CL of phagocytes has been observed in chronic inflammatory disease and can be induced by various serum factors such as monokines and immune complexes. The present study demonstrates an increased CL of blood-borne phagocytic cells in untreated HD. Furthermore, CL of blood monocytes and PMN correlated to tumour burden and histologic subtype, respectively.
Antibody-dependent cell-mediated cytotoxicity to β-lactoglobulin-coated cells with sera from children with intolerance of cow’s milk protein
Authors: SAALMAN R , CARLSSON B , FÄLLSTRÄM S P , HANSON L Å , AHLSTEDT S 
Published: July 2010

SUMMARYThe capacity of serum antibodies against β-lactoglobulin to mediate antibody-dependent cell-mediated cytotoxicity (ADCC) was analysed in sera from children with cow’s milk protein intolerance (CMPI). The children with CMPI were divided into three groups according to clinical features: delayed-onset CMPI with gastrointestinal symptoms (n= 8); immediate-onset CMPI with gastrointestinal and skin symptoms (n= 8); and immediate-onset CMPI with skin symptoms only (n= 8). The CMPI groups were compared with children with untreated (n= 9) or treated (n= 8) coeliac disease and a control group (n= 22). Sera from the children were examined for cytotoxic effects using lymphocytes from healthy adults as effector cells and radiolabelled β-lactoglobulincoated erythrocytes from the same donor as target cells. In addition, IgG and IgA serum antibodies against β-lactoglobulin were determined with ELISA. Sera from children with CMPI and gastrointestinal symptomatology showed a significantly increased capacity to induce ADCC reactivity as compared with controls. This increased capacity was seen in sera from those with immediate as well as delayed onset of the gastrointestinal symptoms. In contrast, sera from children who had an immediate-onset CMPI with only skin symptoms mediated no such increase in ADCC reactivity. Moreover, children with coeliac disease with a few exceptions, demonstrated low ADCC reactivity, despite the fact that they had high levels of antibodies against β-lactoglobulin. ADCC may be an immunopathogenic mechanism in certain cases of CMPI with gastrointestinal symptoms.
Anti-thyroid peroxidase antibodies in sera from healthy subjects and from patients with chronic thyroiditis: differences in the ability to inhibit thyroid peroxidase activities
Authors: KOHNO Y , YAMAGUCHI F , SAITO K , NIIMI H , NISHIKAWA T , HOSOYA T 
Published: July 2010

SUMMARY
A significant percentage (6.4%) of healthy subjects was found to contain anti-thyroid peroxidase (TPO) antibodies in their sera. However, in contrast with IgG from sera of patients with chronic thyroiditis, IgG from sera of healthy subjects did not inhibit TPO activities both in guaiacol and iodide assays. In addition, anti-TPO antibodies from healthy subjects did not block the inhibition of enzyme activities by anti-TPO antibodies from patients. These findings suggest that anti-TPO antibodies from healthy subjects do not bind to the epitopes relating to substrate-combining sites of TPO. Thus, the specificities of anti-TPO antibodies in healthy subjects may differ from those in cases of chronic thyroiditis.
Proliferative and cytotoxic responses to mannoproteins ofCandida albicansby peripheral blood lymphocytes of HIV-infected subjects
Authors: QUINTI I , PALMA C , GUERRA E C , GOMEZ M J , MEZZAROMA I , AIUTI F , CASSONE A 
Published: July 2010

SUMMARYMucosal candidiasis is one of the first opportunistic diseases in HIV-infected subjects. In order to understand the relationship between this disease and immunodeficiency to chemically defined, immunodominant Candida antigens, a mannoprotein fraction from C. albicans cell wall (GMP) was used to analyse proliferative and non-MHC-restricted cytotoxic responses of peripheral blood mononuclear cells (PBMC) from normal and HIV-infected subjects. In the former, GMP induced extensive blastogenesis, generation of powerful cytotoxicity against a tumour cell line (K562), and production of substantial amounts of interferon-gamma (IFN-γ). Cultured PBMC from HIV-infected subjects manifested an early decreased ability for proliferative as well as differentia live cytotoxic responses to the candidal mannoproteins. This inability became clearly evident in subjects with stage III (CDC) of the disease, was total in CDC stage IV and occurred even in some subjects with a normal number of CD4+ cells. Low or absent response to GMP correlated with lack of response to tetanus toxoid. In contrast, both lymphoproliferative and cytotoxic responses to exogeneous IL-2 was highly preserved at all stages of infection. The production of IFN-γ in GMP-stimulated PBMC cultures critically fell to negligible values in most of the subjects in CDC stages II and III. Thus, the lowered or absent cell-mediated immune responses to candidal mannoprotein may be one factor to explain the early, elevated susceptibility of HIV-infected subjects to mucosal candidiasis. This study also shows that our mannoprotein preparation may be used as a probe to detect the overall efficiency of T cell responses in the above subjects.
Beta-casomorphin (BCM) and human colonic lamina propria lymphocyte proliferation
Authors: ELITSUR Y , LUK G D 
Published: July 2010

SUMMARYBCM is a milk-derived peptide with opiate-like properties which is absorbed through the gastrointestinal mucosa. It has been shown to affect gastrointestinal motility, absorption and secretion. Recently, modulation of the immune system by BCM was also reported. In this study we investigated the in vitro effect of BCM on the human mucosal immune response as represented by lamina propria lymphocyte (LPL) proliferation. Results show that BCM significantly inhibited concanavalin A (ConA) stimulated LPL DNA synthesis. BCM also inhibited ornithine decarboxylase activity (ODC) in ConA-stimulated LPL. Although BCM also inhibited 12-O-tetradecanoyl phorbol-13-acetate (TPA) stimulated LPL DNA synthesis, the degree of inhibition was much lower than in ConA-stimulated LPL. The anti-proliferative effect of BCM was reversed by the opiate receptor antagonist, neloxone. Our results suggest that BCM may affect the human mucosal immune system, possibly via the opiate receptor.
Human colonic intra-epithelial lymphocytes are suppressor cells
Authors: HOANG P , DALTON H R , JEWELL D P 
Published: July 2010

SUMMARYHuman colonic intra-epithelial lymphocytes (IEL) suppress the proliferation of autologous lamina propria lymphocytes, but not aulologous peripheral blood mononuclear cells, when stimulated with phytohaemagglutinin. This suppressor function is mediated by a CD8-depcndent soluble factor and is not related to the expression of the γø T cell receptor. These findings may be relevant to the induction of mucosal tolerance. However, there is no defect in suppressor activity of colonic IEL in inflammatory bowel disease.