bluuebunny/crossref_metadata_2025_split huggingface dataset:
Adhesion molecule expression in Graves' thyroid glands; potential relevance of granule membrane protein (GMP-140) and intercellular adhesion molecule-1 (ICAM-1) in the homing and antigen presentation processes
Authors: MIYAZAKI A , MIRAKIAN R , BOTTAZZO G F 
Published: July 2010

SUMMARYTo assess the potential role of adhesion molecules in the pathogenesis of Graves' disease, we examined the expression of several of these adhesion molecules, including intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule (VCAM-1) and granule membrane protein-140 (GMP-140), in sections of Graves' thyroid glands and control thyroids, using Immunohistochemical techniques. Up-regulated expression of GMP-140 was frequently observed on endothelial cells (EC) of post-capilliary venules in all Graves' thyroids examined, compared with an occasional weak staining on EC control glands. Some capillary EC around thyroid follicles (perifollicular EC) were strongly positive for GMP-140 in the Graves' thyroids in contrast to a negative staining on the same Structures in the control glands. In addition, there was a correlation between the reactivity and frequency of GMP-140 expression on EC and the severity of mononuclear cell (MNC) infiltration in the Graves' thyroids. The expression of ICAM-1 was up-regulated on perifollicular EC and EC of small venules in some thyroids of both Graves' and control groups. Conversely, no significant expression was observed on any type of EC for both endothelial-leucocyte adhesion molecule-1 (ELAM-1) and VCAM-1. However, dendritic-like cells, present within lymphocytic infiltrates, were positive for VCAM-1 in most of the Graves' thyroids examined, especially in those with a severe lymphocytic infiltration. Thyrocytes were constantly negative for the expression of all tour adhesion molecules investigated. These data suggest that GMP-140, as well as ICAM-1, could play an important role in the initiation of MNC infiltration in Graves' disease. ELAM-1 and VCAM-1 appear not to be relevant for the migration of MNC from the blood vessels into the target gland, although VCAM-1 expression on dendritic-like cells might play an additively tissue-selective role in autoantigen presentation and subsequent elicitation of autoimmune phenomena.
Distribution of retroviral p15E-related proteins in neoplastic and non-neoplastic human tissues, and their role in the regulation of the immune response
Authors: SCHEEREN R A , OOSTENDORP R A J , VAN DER BAAN S , KEEHNEN R M J , SCHEPER R J , MEIJER C J L M 
Published: July 2010

SUMMARYIn patients with head and neck carcinomas and in patients with chronic purulent upper airway infections, low molecular weight retroviral p15E-like factors are found. These factors are responsible for partial defects in the cellular immune response. We studied the distribution of these p15E-related proteins in neoplastic. inflamed and normal human tissues and related these findings with the presence of p15E-like factors in patients's era. Demonstration of p15E-like proteins in sera of patients with upper airway infections and of patients with head and neck carcinomas correlated exclusively with the presence of p15E in normal and pathologic epithelium of the upper respiratory tract, p15E was not demonstrated in epithelia of other localizations. Our results suggest that chronic stimulation or neoplastic transformation of the epithelia of the upper respiratory tract stimulates the production of p15E-like proteins leading to their reported immunosuppressive actions.
Secretion of Toxoplasmagondii-specfic antibodyin vitroby peripheral blood mononuclear cells as a new marker of acute toxoplasmosis
Authors: VENDRELL J P , PRATLONG F , DECOSTER A , BOULOT P , CONGE A M , DARCY F , SEGONDY M , HUGUET M F , SERRE A 
Published: July 2010

SUMMARYAntigen-specific antibody secretion in vitro by peripheral blood mononuclear cells (PBMC) reflects an in vivo stimulation of the immune system by the antigen. Primary infection of immunocompetent patients with T. gondii causes an acute infection followed by chronic toxoplasmosis. We examined in vitro anti-Toxoplasma antibody production by PBMC during the acute and chronic phases of toxoplasmosis. PBMC from patients with acute or chronic toxoplasmosis and seronegative subjects were cultured for up to 6 days. Anti-Toxoplasma antibodies were assayed in supernatants by ELISA and immunoblotting. Anti-Toxoplasma antibodies were detected in supernatants of PBMC from 29 pregnant women who seroconverted during gestation. PBMC from 17 patients who had chronic toxoplasmosis and PBMC from 10 seronegative healthy controls did not secrete Toxoplasma-specific antibodies. This in vitro antibody secretion was spontaneous, active and transient since it disappeared between 11 and 24 weeks after seroconversion. Anti-Toxoplasma antibody secretion by PBMC from patients with acute toxoplasmosis is consistent with an in vivo stimulation of the immune system by T. gondii antigens. Our results represent a new approach for studying the immunological response during T. gondii infection and could have important implications for the diagnosis of acute and re-activated toxoplasmosis.
Clonality of T lymphocytes expanded with IL-2 from rheumatoid arthritis peripheral blood, synovial fluid and synovial membrane
Authors: CANTAGREL A , ALAM A , COPPIN H L , MAZlERES B , De PREVAL C 
Published: July 2010

SUMMARYThe association of rheumatoid arthritis (RA) with particular MHC class II genes suggests that autoantigen-spccific T cell clones present in joints could be central to the pathogenesis of the disease. Previous investigations on the clonal diversity of T cells infiltrating the rheumatoid synovial membrane have yielded conflicting results. With the use of Southern blot analysis, we investigated the clonalily of rheumatoid T cell lines expanded from peripheral blood, synovial fluid and synovial tissue. From peripheral blood lymphocyte (PBL) of RA patients and healthy normal controls, we also checked the consequences of two different culture conditions on the clonality of these cell lines. From control PBL, we found that in vitro non-specific expansion of non-clonal T cell populations does not create artefactual clonal selection. However, growing T cells in vitro with IL-2 seems to be able to lead to preferential expansion of cells bearing IL-2 receptor (IL-2R). We identified such in vivo activated IL-2-sensitive T cell clones frequently in RA synovial tissue (8/13) and more rarely in synovial fluid and peripheral blood (3/12). One patient presents the same T cell receptor gene rearrangements in synovial membrane of two affected joints. In RA synovial tissue, the frequency of these IL-2-responsive T cells is most prevalent among actively inflamed membranes removed early in the disease process. The role and the relevance to the disease of these I L-2-responsivc T cells remain to be elucidated.
Cell-mediated transfer of collagen-induced arthritis in mice and its application to the analysis of the inhibitory effects of interferon-gamma and cyclophosphamide
Authors: NAKAJIMA H , HIYAMA Y , TAKAMORI H , TSUKADA W 
Published: July 2010

SUMMARYWe developed a convenient and reliable procedure for the cell-mediated passive transfer of type II collagen (Cll)-induccd arthritis (CA). Spleen cells from DBA/1 mice with CA were intravenously transferred into syngeneic recipient mice. Arthritis developed only in those recipients which had received whole-body x-irradiation (8 Gy) just before cell iransfer and intrapcritoneally given soluble CII without adjuvant immediately after transfer. Non-immunized splenocytes could not induce arthritis even in irradiated recipients given soluble CII. Development of arthritis depended on the number of cells transferred; 5 ± 107 cells induced severe and long-lasting arthritis in every recipient approximately 10 days after transfer. Severity of this arthritis was clinically and histologically similar to classical CA in donors. Arthritogenic splenocytes were generated in donors no later than 20 days after priming with CII in Freund's complete adjuvant, when arthritis had yet to occur, and were detected for more than 5 weeks. One splenocyte population responsible for transferring arthritis was CD4+ T cells. We then applied this system to show that prophylactic treatment of CII-immunized mice with cyclophosphamide (CY. 7 mg/kg), but not interferon-gamma (IFN-γ. 105 U/mouse), suppressed the arthritogenic ability of their spleen cells, although both treatments inhibited the development of CA. Treatment of recipients with IFN-γ, however, inhibited the development of arthritis upon transfer with CII-immunized splenocytes. These results indicate that CY and IFN-γ act at the induction and effector phases of arthritogenic lymphocytes, respectively. Thus, this system facilitates investigation of pathological mechanisms of CA, and of mechanisms of anti-arthritics.
Comparison between the protective effects of mycobacterial 65-kD heat shock protein and ovomucoid in pristane-induced arthritis: relationship with agalactosyl IgG
Authors: GHORAISHIAN M , ELSON C J , THOMPSON S J 
Published: July 2010

SUMMARYThe IgG of patients with rheumatoid arthritis and mice with pristane induced arthritis (PIA) lends to lack the terminal galactose normally on the conserved N-acetylglucosamine linked β1–2 to mannose in IgG. The terminal N-acetylglucosamine (GlcNAc) residues of oligosaccharides on agalactosyl IgG may be an important component of the action of these glycoforms. Here, administration of ovomucoid, a glycoprotein rich in terminal GlcNAc, before pristane injection was found to reduce the incidence of PIA. This observation is the second report of an intraperitoneally administered antigen that reduces the incidence of PIA. mycobacterial 65-kD heat shock protein (hsp65) being the first. The suppressive effect of ovomucoid was not transferred from protected to naive recipients by spleen cells at the dose tested. By contrast, transfer of spleen cells from hsp65-protected mice to naive recipients conferred protection and this protection may be antibody-mediated. It is considered that ovomucoid and hsp65 protect against the development of PIA by different mechanisms.
Critical role of peripheral blood phagocytes and the involvement of complement in tumour necrosis factor enhancement of passive collagen-arthritis
Authors: FAVA R A , GATES C , TOWNES A S 
Published: July 2010

SUMMARYStudies have implicated tumour necrosis factor-alpha (TNF-α) in type-II collagen (CII)-induced arthritis (CIA), a well established animal model of human rheumatoid arthritis. Precisely how TNF is involved in CIA is not yet clear. In this study the effects of TNF on CIA were examined, independent of its potential effects on the immune response, by performing peri-articular injection of TNF in combination with passive immunization of rats. A sub-arthritic dose (5 mg) of affinity-purified anti-CII IgG, which alone was insufficient to induce spontaneous clinical arthritis, was used throughout the study. Obvious clinical arthritis that persisted for several days was rapidly induced by injections of 100 ng TNF into hindpaws of rats that were passively immunized shortly before the TNF injection. Injections of TNF in non-immunized control rats did not induce clinical arthritis, nor did buffer-only injections in passively immunized controls. The clinical arthritic response was a local phenomenon, limited only to the TNF-injected hindpaws. No swelling was observed in the opposite, buffer-injected hindpaws, indicating the effects of TNF were not systemic. Depletion of peripheral blood phagocytes with anti-rat neutrophil antiserum before passive immunization completely abolished the ability of TNF to induce clinical arthritis, identifying phagocytic cells as the essential target cells in evoking this arthritic response. A role forcomplement activation was also demonstrated in this model through the use of a soluble recombinant version of CD35, the cell surface complement receptor type-1 (sCRl, BR155730), which significantly reduced TNF-induced arthritis in phagocyte-replete rats.
Activation of human complement by mouse and mouse/human chimeric monoclonal antibodies
Authors: SEINO J , EVELEIGH Ph , WARNAAR S , van HAARLEM L J M , van ES L A , DAHA M R 
Published: July 2010

SUMMARYThe complement (C)-activating capabilities in human serum of 32 mouse and 10 mouse/human chimeric MoAbs of different isotypes, and their fragments, were tested in vitro. Activation of C via the classical pathway (CP) was performed in 1% factor D-deficient serum in gelatin containing Veronal buffer in the presence of calcium and magnesium (GVB++), while activation of the alternative pathway of C (AP) was assessed in 10% Clq-depleted serum in the presence of 5 mm MgCl2 in GVB++. The C-activating ability of MoAbs was expressed relative to the degree of activation of complement by aggregated IgG for the CP and relative to mouse IgG 1 for the AP. All of seven mouse IgG2a MoAbs were potent activators of the CP. The results of CP activation by IgG1, IgG2b and IgG3 isotypes were different for individual MoAbs. Only three (two IgG 1 and one IgG3) of 32 mouse MoAbs were potent activators of the AP. IgG2a and IgG2b were relatively poor AP activators. There were a few MoAbs which activated both the AP and CP. Of 10 chimeric MoAbs, two IgG1, one IgG2 and one IgG4 were poor or non-activators of the CP. On the other hand, IgG2 and IgG4 were good AP activators. IgG3 was the most potent AP activator. Most of the F(ab')2 fragments were activators of the AP and displayed no activation of the CP. Fc fragments only activated the CP. whereas Fab'did not activate the CP or the AP. These studies suggest that the route of complement activation by class and subclass MoAbs can not always be predicted in advance and based only on their subclass identity.
Localization of tumour necrosis factor-alpha (TNF-α) and its receptors in normal and psoriatic skin: epidermal cells express the 55-kD but not the 75-kD TNF receptor
Authors: KRISTENSEN M , CHU C Q , EEDY D J , FELDMANN M , BRENNAN F M , BREATHNACH S M 
Published: July 2010

SUMMARYThe distribution of TNF-α, p55 TNF receptor (TNF-R) and p75 TNF-R in normal skin and uninvolved and lesional skin from psoriasis patients has been investigated, using specific mono- and polyclonal antibodies. In normal skin, and uninvolved and lesional skin from psoriasis patients, p55 TNF-R is associated with epidermal keratinocytes and a network of upper dermal dendritic cells. This suggests that the actions of TNF-a on epidermal cells in vivo are mediated by binding to the p55 TNF-R. In lesional psoriasis skin, there was staining of the parakeratotic stratum corncum and increased expression of p55 TNF-R in association with upper dermal blood vessels. Staining for p75 TNF-R in normal skin was restricted to eccrine sweat ducts and dermal dendritic cells, and was absent from the epidermis. In lesional psoriasis skin, there was staining for p75 TNF-R in association with upper dermal blood vessels and perivascular infiltrating cells. TNF-α in normal skin was predominantly localized to the basal cell layers of the epidermis, and was seen in association with eccrine ducts and sebaceous glands. In lesional psoriasis skin, and to a lesser extent in uninvolved psoriasis skin. TNF-α was distributed throughout the epidermis, and was also specifically localized to upper dermal blood vessels. Up-regulation of TNF-α. p55 TNF-R and p75 TNF-R on dermal blood vessels in psoriasis may play an important role in the pathogenesis of this condition by promoting cutaneous recruitment of inflammatory cells.
Prognostic value of phenotypic alterations in blood lymphocyte subsets in a murine retrovirus-induced immunodeficiency syndrome (MAIDS)
Authors: CHAU F , LEVACHER-CLERGEOT M , DESFORGES B , RICATTE L , SINET M 
Published: July 2010

SUMMARYMice infected with the Duplan strain of murine leukaemia virus (Dup MuLV), a retrovirus, develop a syndrome sharing several features with AIDS, including lymphadenopathy and profound immunodeficiency. We measured the changes in peripheral blood lymphocyte populations and evaluated their predictive value for the outcome of disease in C57B1/6 mice. Animals were inoculated with Dup MuLV (SCI /Dup MuLV confluent fibroblast supernatant or spleen extract from an infected mouse). Peripheral blood lymphocyte subsets were sequentially monitored for 73 days using flow cytometric analysis and MoAbs directly conjugated to fluorochromes. A striking fall in the Thy 1.2 cell count occurred in diseased animals, mostly affecting the CD8+ cell compartment. At the same time, the percentage of Ly5+ cells was increased. Mice were killed at day 73 and spleen and lymph node lymphocytes were analysed. Phenotypic lymphocyte modifications in peripheral blood were closely related to those in the spleen or lymph nodes. Analysis of Ly6c antigen expression on CD4+ and CD8+ cells showed a selective expansion of the CD8+ Ly6c+ subset, which may reflect a state of immune activation. Our results suggest that phenotypic alterations of peripheral blood lymphocytes are a good marker of disease progression in this model and could be a useful criterion to evaluate antiretroviral therapy.
Interactions of anti-DNA antibodies with Z-DNA
Authors: KRISHNA P , FRITZLER M J , Van de SANDE J H 
Published: July 2010

SUMMARYSystemic lupus erythematosus (SLE) sera, two classes of serum lipoproteins, and IgG antibodies from SLE and normal sera were tested for their reactivity with a Z-DNA polymer, Br-poly (dG-dC). In all cases preferential binding to Z-DNA over B-DNA was observed. This interaction, for the most part, could be inhibited by the negatively charged phospholipid, cardiolipin, which suggests that most of the anti-Z-DNA activity associated with sera arises from relatively non-specific ionic interactions between proteins and polyanionic molecules. An assay has been described that can eliminate proteins cross-reactive with negatively charged phospholipids.
Lower antibody response to tetanus toxoid associated with higher auto-anti-idiotypic antibody in old compared with young humans
Authors: ARREAZA E E , GIBBONS J J , SISKIND G W , WEKSLER M E 
Published: July 2010

SUMMARYThe production of anti-tetanus toxoid (TT) antibody and anti-anti-TT (auto-anti-Id) antibody has been measured in three young and three old persons. Both antibodies were measured using ELISA. We found that: (i) the anti-TT response of old subjects was lower than that of young subjects, (ii) scrum auto-anti-Id antibody concentration was higher in old compared with young humans before boosting with TT, and (iii) anti-TT antibodies from different humans shared Id cross-reactivity when tested with a rabbit anti-Id antibody. Thus, the serum anti-TT antibody response to boosting was inversely correlated with the serum level of auto-anti-Id. This conclusion is consistent with the view that the higher level of auto-anti-antibody in older subjects contributes to their impaired antibody response to TT.
Polynucleotide specificity of anti-reactive oxygen species (ROS) DNA antibodies
Authors: ARA J , ALI R 
Published: July 2010

SUMMARYHydrogen peroxide in the presence of short wavelength UV light was able to induce alterations in native DNA fragments of 300 bp (ROS-DNA). thereby rendering it immunogenic in experimental animals. The specificity of induced antibodies was investigated by direct binding and competition ELISA. Inhibition studies revealed nearly 89% inhibition in the antibody binding by the immunogen and recognition of native B-, A- and allied conformations presented by various synthetic polynucleotides. Gel retardation assay reiterated the formation of immune complexes between induced antibodies and native and ROS-DNA fragments. It was observed that naturally occurring anti-DNA autoantibodies from systemic lupus erythemalosus(SLE) sera recognize ROS-DNA. The comparison of the specificities of anti-DNA auloantibodies from 10 SLE patients showed a 20–50-fold preference for ROS-DNA over native DNA. These results demonstrate that anti-DNA antibodies can be induced by ROS-DNA, and that some of the autoimmune DNA binding antibodies found in SLE may result from response to reactive oxygen species.
Modulation of α1-acid glycoprotein (AGP) gene induction following honey bee venom administration to adjuvant arthritic (AA) rats; possible role of AGP on AA development
Authors: YIANGOU M , KONIDARIS C , VICTORATOS P , HADJIPHTROU-KOUROUNAKIS L 
Published: July 2010

SUMMARYHoney bee venom (HBV) administration to adjuvant arthritic (AA) rats resulted in a significant suppression of arthritis and in suppression of the hepatic acute phase α1-acid glycoprotein (AGP) gene induction at the early stages of disease development. AGP administration in AA rats resulted in acceleration of arthritis development and in increase of severity and duration of the disease. IL-1, IL-6. tumour necrosis factor (TNF) and glucocorticoids alone are not responsible for thc HBV-mediated AGP gene down-regulation. These results indicate that AGP gene expression in AA and HBV-treated AA rats involves the interaction of several factors, and that AGP plays a role for AA development in rats.
Circulating monocytes are activated in newly diagnosed type 1 diabetes mellitus patients
Authors: JOSEFSEN K , NIELSEN H , LORENTZEN S , DAMSBO P , BUSCHARD K 
Published: July 2010

SUMMARYInvestigations in the BB rat and the non-obese diabetic (NOD) mouse have provided substantial evidence for the involvement of the monocyte/macrophage system in the development of type 1 diabetes mellitus. However, it is not known whether monocytes play the same role in the pathogenesis of human type 1 diabetes. We investigated this problem in a longitudinal study of 29 recent-onset type 1 diabetes mellitus patients. Monocyte chemotaxis, phagocytosis and superoxide production as well as metabolic and haematological parameters were studied immediately after diagnosis and 6 months later. At diagnosis the patients had activated casein and C5a chemotaxis (casein 70 ± 9 versus 150 ± 5 (mean ± s.e.m.), P &lt; 0001; C5a 137 ± 10 versus 158 ±5, P &lt; 005 (activation immobilizes monocytes, reducing the measured values)), and activated superoxide production (3·6 ± 03 versus 3·0 ± 03, P &lt; 0·05), After 6 months casein chemotaxis (115 ±16 versus 150 ±5, P &lt; 005) and Candida phagocytosis (33 ±01 versus 2·8 ±0·2. P &lt; 0.001) were still activated. There was no correlation with other clinical or paraclinical parameters. We conclude that the circulating monocytes in newly diagnosed type 1 diabetes patients are activated. It is reasonable to expect that monocytes at the local site of inflammation in pancreas are even further activated. This could play a pathogenic role in β cell destruction.