bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inhibitory effect of 11β-hydroxypregna-l,4-diene-3,20-dione (ΔHOP) on lymphocyte proliferation
Authors: RONDINONE C M , SCHILLACI R , CASTILLO M B , ROLDÁN A 
Published: July 2010

SUMMARYWe have compared the immunosuppressive effect of ΔHOP and glucocorticoids on lymphocyte proliferation and IL-1 secretion. The new synthetic steroid only inhibited proliferation of phytohaemagglutinin (PHA)-stimulated human lymphocyte at high concentrations and the effect did not persist after washing out the steroid- In contrast, glucocorticoids produced the classical dose-response inhibition and the effect persisted when they were removed from the cultured medium. Although both steroids decreased IL-1 secretion from human monocytes stimulated with lipopolysaccharide (LPS), they exert the same effect through a different mechanism. The experiments we report suggest that the decrease of IL-1 synthesis produced by ΔHOP could be caused by inhibition of LPS phagocytosis. These results support our hypothesis that ΔHOP exerts its immunosuppressive and anti-inflammatory effect by a non-genomic mechanism.
Piroxicam, indomethacin and aspirin action on a murine fibrosarcoma. Effects on tumour-associated and peritoneal macrophages
Authors: VALDÉZ J C , PERDIGÓN G 
Published: July 2010

SUMMARYGrowth of a methylcholanthrene-induced fibrosarcoma in BALB/c mice was accompanied by an increase in the activation state of tumour-associated macrophages (TAM). as measured by their FclgG receptor expression, phagocytic index and β-glucuronidase levels. All of these parameters were markedly higher in TAM than in peritoneal macrophages (PM) derived from the same animal. On the other hand, PM from tumour-bearing mice showed lower activation parameters than PM from normal animals. We also studied the effect on tumour development of three inhibitors of prostaglandin synthesis: indomethacin. piroxicam and aspirin. Intraperitoneal administration of these drugs during 8 d was followed by the regression of palpable tumours. Indomethacin (90 mg/d) induced 45% regression, while with piroxicam (two 400 mg/d doses and six 200 mg/d doses) and aspirin (1 mg/d) 32% and 30% regressions, respectively, were observed. The growth rate of non-regressing tumours, which had reached different volumes by the end of the treatment, was delayed to a similar extent by the three anti-inflammatory non-steroidal drugs (NSAID). With respect to TAM, the treatment did not induce any significant change in their activation state, though both piroxicam and indomethacin increased slightly the TAM number. In contrast, NSAID administration was followed by a remarkable increase in the activation parameters of PM when compared with PM from tumour-bearing mice receiving no treatment. Indeed, these parameters were in some cases higher than those of PM from normal mice. The leukocytosis (60 000/μl) with neutrophilia (80%) induced by tumour growth on peripheral blood leukocytes (PBL) was reversed by the treatment to values close to normal, in parallel with the reduction of tumour size. A drop in haematocrit was also noted which was most probably a consequence of tumour growth rather than of the treatment. This study reveals that the three NSAID tested have a remarkable antitumour activity, which correlates with the restoration of PM activity and PBL values.
Immune complex binding efficiency of erythrocyte complement receptor 1 (CR1)
Authors: MADI N , PACCAUD J-P , STEIGER G , SCHIFFERLI J A 
Published: July 2010

SUMMARYC3b-coated immune complexes adhere to the complement receptor I (CR1. CD35) on human erythrocytes. This multi-valenl binding might be favoured by the known clustering of CR1 and by the multiple C3b-binding sites on each CR1. The size of the CR1 clusters correlates directly with the number of CR1 /erythrocytes, and the different structural CR1 alleles bear between two and five C3b-binding sites. Using radiolabelled hepatitis B surface antigen-antibody complexes, we investigated whether CR1 numbers and structural alleles modulate the ability of erythrocytes to bind immune complexes, and assessed if any reorganization of immune complexes takes place at the erythrocyte surface after the initial binding reaction. The binding efficiency (immune complexes/CR1) correlated with CR1 number as determined by the maximal binding at 4°C, the kinetics of binding at 37°C, and the binding in the presence of excess immune complexes and of immune complexes of small size. Binding efficiencies were similar for erythrocytes with low CR1 from normal subjects and patients with AIDS or SLE. A monoclonal antibody blocking the C3b-binding sites (3D9) of CR1 interfered with binding efficiency at a lower concentration on cells bearing low CR1 numbers, suggesting that CR1 clustering is essential. The larger alleles of CR1 (DD and BB) were more efficient than AA alleles. The distribution of immune complexes, visualized by immunofluorescence, was heterogeneous on erythrocytes: about two out of three cells bore between one and 12 immune complexes. No visible immune complex reorganization took place after initial binding, as prefixed erythrocytes displayed the same immune complex distribution and number/erythrocytes as unfixed erythrocytes. The contribution of CR1 alleles in immune complex binding efficiency was confirmed by morphological analysis. These results demonstrate that immune adherence efficiency is the resultant of the CR1 clustering, as well as the particular alleles carried by erythrocytes. Moreover, there is little or no immune complexes surface reorganization after the initial binding reaction.
Cellular origins of serum complement receptor type 2 in normal individuals and in hypogammaglobulinaemia
Authors: LING N , HANSEL T , RICHARDSON P , BROWN B 
Published: July 2010

SUMMARYA soluble form of complement receptor 2 (sCR2) is found in normal human serum. Amounts present arc about 30 90 ng/ml, which is of the same order as reported tor soluble CR1. Although B cells express surface CR2 and are the main peripheral blood source of sCR2 they do not appear to be the major tissue source of serum sCR2. Scrum levels of sCR2 of patients with hypogammaglobulinaemia were not significantly different from those of normal individuals even in the case of two brothers with Bruton's X-linked agammaglobulinaemia (XLA) lacking (CD 19+) B cells. On gel filtration through Sephacryl S-300 the sCR2 from XLA serum behaved exactly like sCR2 from normal serum or sCR2 affinity purified from cell supernates of a B lymphoblastoid line or from the T-ALL line MOLT-4. In all cases a single peak appeared at the same point in the chromatogram. Possible alternative sources of serum sCR2 are follicular dendritic cells (FDC) which are known to express CR2 strongly and T6+ lymphocytes within the thymus. Peripheral T cells from adults have not been reported to express CR2. However, investigation showed that cells from the Bruton's XLA cases produced small amounts of sCR2 in culture and although no CD21 was detected on the surface of the mononuclear cells by flow cytometry, the more sensitive direct antibody rosette test readily detected CD21. Further studies showed that non-B cells from control samples of cord blood or blood of young children also weakly expressed CD21.
Severe combined immunodeficient (SCID) mice: a model for investigating human thyroid autoantibody synthesis
Authors: MACHT L , FUKUMA N , LEADER K , SARSERO D , PEGG C A S , PHILLIPS D I W , YATES P , MCLACHLAN S M , ELSON C , SMITH B REES 
Published: July 2010

SUMMARYWe have studied the ability of lymphocytes from the blood, thyroid and lymph nodes of patients with autoimmune thyroid disease (AITD) to produce auloantibodies to thyroglobulin (Tg) and/or thyroid peroxidasc (TPO) in SCID mice. Human IgG class Tg and/or TPO antibodies were detectable in plasma from SCID mice 7 days after transfer of 15–25 × I06 cells mouse and the highest levels were recorded 2–3 weeks later. In contrast, Tg and/or TPO antibodies were undctcctablc in recipients of lymphocytes from thyroid antibody negative controls. AITD thyroid lymphocytes produced the most antibody in recipient mice and lower levels were observed in recipients of AITD blood and lymph node lymphocytes. The amounts of Tg and or TPO antibody detected were in accordance with the ability of thyroid and lymph node lymphocytes to secrete these autoantibodies spontaneously in culture (indicating the presence of cells activated in the patient) and with the capacity of blood lymphocytes (probably B memory cells) to secrete Tg and or TPO antibodies in culture in response to pokeweed mitogen. Tg antibodies in plasma from SCTD recipients of thyroid lymphocytes were of subclasses IgG1, IgG2 and IgG4 and the proportions closely resembled those of the donor's scrum Tg antibodies. Blood lymphocytes transferred to SCiD recipients were also able to produce Tg antibodies of subclasses1, 2 and 4 but the subclass distribution varied between mice and the reason for this is not clear at present. Since SCID mice provide an environment in which B lymphocytes from patients with AITD can be activated without mitogen to secrete thyroid antibodies, this model will provide a powerful system for elucidating the mechanisms regulating the secretion of human antibodies to Tg and TPO.
Peripheral blood and synovial fluid T cells differ in their response to alloantigens and recall antigens presented by dendritic cells
Authors: STAGG A J , HARDING B , HUGHES R A , KEAT A , KNIGHT S C 
Published: July 2010

SUMMARYProperties of T cells from inflammatory lesions were analysed by comparing the response of peripheral blood (PB) and synovial fluid (SF)T cells from 19 patients with a range of arthropathies to enriched allogeneic dendritic cells (DC) in a primary mixed leucocyte reaction (MLR). In 17 patients the proliferative response of SF T cells was significantly (P &lt; 0.05) less than that of PB lymphocytes. The reduced response of SF T cells was observed in all disease categories studied and could not be attributed to differences in cell number requirements or response kinetics. Addition of recombinant interlcukin-2 enhanced the response of SF T cells in a dose-dependent manner. Cell mixing experiments suggested that active suppression was not the underlying mechanism of the poor MLR response of SF T cells. In contrast to the MLR response, SF T cells were able to mount vigorous proliferative responses to recall antigen presented by autologous antigen-presenting cells. The possibility is discussed that T cells compartmentalized at inflammatory lesions are a unique population with a diminished ability to interact with DC and respond to primary stimuli but an ability to respond to secondary antigenic challenge.
Antibody penetration of viable human cells. I. Increased penetration of human lymphocytes by anti-RNP IgG
Authors: MA J , CHAPMAN G V , CHEN S-L , MELICK G , PENNY R , BREIT S N 
Published: July 2010

SUMMARYAntibody penetration of viable cells and interaction with intracelluiar antigens may have major consequences for immunopaihological processes in connective tissue diseases. We have reported previously that antibody can penetrate viable human lymphocytes. To assess further the role of antinuclear antibodies in this process, peripheral blood lymphocytes (PBMC) were incubated with FITC-conjugated IgG fractions from sera containing anti-RNP (anti-RNP IgG), Ro(SS-A), La(SS-B) and dsDNA antibodies and control sera for 24 h. Using crystal violet to quench cell surface staining, intracellular fluorescence of viable lymphocytes was quantified on the flow cytomcter. It was noted that anti-RNP IgG entered 46.4±7.2% of lymphocytes which was significantly higher than anti-Ro(SS-A) (29.9±4.1%, P &lt; 0.05), La(SS-B) (22.0±7.5%, P &lt; 0.01) IgG and control IgG (28.8±2.1%, P &lt; 0.05) and not statistically different from anti-dsDNA IgG (32.6±14.3%). Inhibition experiments showed that the increased number of cells penetrated by anti-RNP IgG was a specific process. Time-course studies showed that anti-RNP IgG entry into cells was different from pooled control IgG. With anti-RNP IgG, positive-staining lymphocytes gradually increased in number from 12 to 24 h incubation, whilst with pooled control IgG, the peak was reached within 5 min. Dual staining experiments suggested that whereas both anli-RNP IgG and pooled control IgG entered Band NK. cells, anti-RNP IgG also entered T cells. Using IgG F(ab')2 and Fc fragments from either anti-RNP IgG or pooled control IgG to compete with their FITC-conjugated counterparts indicated that the entry of anti-RNP IgG into viable cells appeared to involve both F(ab')2 and Fc fragments, and pooled control IgG depended exclusively on the Fc portion of IgG. Further investigation by incubating anti-RNP IgG with 35S-methionine-labelled monocyte-depleted PBMC (MD-PBMC) suggested that anti-RNP IgG might react with the corresponding antigens either on the cell surface or within the cytoplasm.
Detection of endogenous cytokines in sera or in lymph nodes obtained from patients with sarcoidosis
Authors: ASANO M , MINAGAWA T , OHMICHI M , HIRAGA Y 
Published: July 2010

SUMMARY
To investigate the possible role of endogenous cytokines in the immunopathogenesis of sarcoidosis, a study of cytokines in lymph nodes obtained from patients with active pulmonary sarcoidosis was carried out using immunoperoxidase staining and radioimmunoassays (RIA). Cells stained for inlerfcron-y (IFN-γ) and tumour necrosis factor-α (TNF-α), which appeared to be CD3+ cells and CD14+ cells, respectively, were seen scattered around granulomas. In contrast, cells positive for intcrlcukin-1β (IL-1β) were located in CD11c+ cells within granulomas. Lymph nodes of patients with sarcoidosis contained significantly higher amounts of IFN-y, TNF-a and IL-1β than control lymph nodes. The levels of IFN-γ and TNF-α in extracts of lymph nodes were correlated with the histological status of the granulomas. IFN-γ was delected in all stages, while the highest level of TNF-α was obtained from lymph nodes containing many active granulomas. The level of serum IFN-γ was always lower than in lymph node extract and correlated significantly with either serum angiotensin-converting enzyme or serum lysozyme. Patients with positive gallium-67 uptake or bilateral hilar lymphadenopathy had high levels of either serum IFN-γ or lysozyme. These results suggest that quantitative analyses of IFN-γ and TNF-α in sera and lymph nodes may serve to elucidate the pathophysiology of sarcoidosis.
Autoantibodies to DNA topoisomerase II in juvenile rheumatoid arthritis
Authors: ZUKLYS K L , SZER I S , SZER W 
Published: July 2010

SUMMARYSera from 58 children with juvenile rheumatoid arthritis were examined for the presence of antibodies to DNA topoisomerase II. Eight sera were reactive in immunoblotting with purified human topoisomerase II and a protein encoded by a cloned cDNA expressed in Escherichia coli which represents the carboxy-terminal domain of the human enzyme. In addition, the sera detect topoisomerase II in mitotic chromosomes and chromosome scaffoids. Five of the sera bind to the native enzyme in solution and deplete such solutions of the active enzyme. All eight sera also contain antibodies to nuclear antigens other than topoisomerase II.
Differential staining of human αβ and γδ T cells by the fluorescein conjugate of an anti-CD3 monoclonal antibody
Authors: MULLERSMAN J E , WHITE G , TUNG K S K 
Published: July 2010

SUMMARYThe enumeration of total T cells, an important function of the clinical immunology laboratory, utilizes antibodies to CD3, the macrornolecular complex associated with the antigen-specific receptors of T cells. We compared the ability of some commonly employed commercial anti-CD3 reagents to stain human peripheral blood lymphocytes. Surprisingly, the fluorescein isothiocyanate (FTTC) conjugate of Coulter clone T3 (FITC-T3) stained most T cells brightly, but selectively stained γδ T cells very dimly or not at all. In contrast, the other anli-CD3 reagents studied (FITC-Leu 4, PE-T3, PE-Leu 4, and indirectly labelled T3 and Leu 4) stained all T cells equivalently. Dual-colour flow cylometric analysis wilh FITC -T3 and PE-Leu 4 readily demonstrated a F1TC-T3 /PE-Leu 4+ population of T cells. This unique population stained dimly or not at all with a combination of anti-CD4 and anti-CD8 monoclonal antibodies and positively with the pan-γδ T cell antibody TCR(5I. Moreover, an excellent correlation was found between the number of FITC-T3 /PE-Leu 4+ cells and the number of TCRδ1+ cells in 32 normal individuals. Thus, the FITC-T3- /PE-Leu 4+ phenotype accurately marks all γδ T ceils. In contrast to FITC T3. both PE-conjugated and unconjugated T3 stained γδ T cells brightly. Therefore, T3 binds to an epitope present on all T cells, but fluoresceinylalion specifically attenuates this antibody’s ability to bind to γδ T cells. These findings indicate that the use of FITC-T3 can result in a significant and variable underestimation of peripheral blood T cell number and demonstrate further that the CD3 complexes of human αβ and γδ T cells are significantly different.
Increased levels of soluble low-affinity Feγ receptors (IgG-binding factors) in the sera of tumour-bearing mice
Authors: LYNCH A , TARTOUR E , TEILLAUD J L , ASSELAIN B , FRIDMAN W H , SAUTÉS C 
Published: July 2010

SUMMARYSoluble forms of low affinity Feγ receptors (FcyR), also called IgG-binding factors (IgG-BF), have been shown to play a regulatory role in immune responses. By using an immunodot assay with the anti-mouse FcyR MoAb, 2.4G2, the levels of IgG-BF have been measured in the sera of mice bearing syngeneic tumours of lymphoid or non-lymphoid origin or in mice injected with high doses of murine IgG. These sera contained large amounts of IgG-BF as compared with controls. In the case of mice bearing IgG2a- or IgG2b-secreting hybridomas or lymphomas, serum IgG-BF increased progressively with tumour size and serum monoclonal IgG concentration, reaching 4–12 times the normal levels. A less than three-fold increase was found in mice bearing an IgG1-secreting hybridoma or tumours which do not secrete IgG (IgA-secreting hybridoma, non-immunoglobulin-secreting lymphoid tumours or melanoma) or in mice injected with 9 mg of monoclonal IgG2a. The enhancement of serum IgG-BF levels was independent of the expression of FcγR by the tumour cells, suggesting that the majority of IgG-BF secreted in response to tumours was produced by the host rather than by the tumour. The increased production of IgG-BF may participate in the control of tumour growth and in the modulation of the host immune responses in tumour-bearing animals.
Thymus lymphocytes in uraemic rats and the effect of thymosin fraction 5in vivo
Authors: IKEMOTO S , KAMIZURU M , HAYAHARA N , OKAMOTO S , WADA S , KISHlMOTO T , MAEKAWA M 
Published: July 2010

SUMMARYThymus lymphocyte subsets in uraemic rats were studied using monoclonal antibodies. Severe and moderate uraemia was induced in rats, and sham-operated and normal rats were used as the controls. As a result, the weight of the thymus decreased in uraemic rats. As for lymphocyte subsets, the frequency of W3/25+OX8+ decreased and those of W3/25−OX8−, W3/25+OX8− and W3/25−OX8+ relatively increased in uraemic rats. All these changes were more significant in severely uraemic than in moderately uraemic rats. When thymosin fraction S (TF5) was administered to severely uraemic rats, the weight of the thymus increased and the lymphocytes subsets normalized. These results suggest that uraemia may cause a maturational impairment of thymus lymphocytes by the depression of thymic hormone secretion.
Study of CYP2D6 gene in children with autoimmune hepatitis and P450 IID6 autoantibodies
Authors: YAMAMOTO A M , MURA C , MORALES M G , BERNARD O , KRISHNAMOORTHY R , ALVAREZ P 
Published: July 2010

SUMMARY
Cytochrome P450 IID6 is an autoantigen recognized by the sera of children affected with a subtype of autoimmune hepatitis. It was hypothesized that a mutation in the CYP2D6 gene could explain the autoimmune response in these patients. To examine this question, genomic DNA from peripheral lymphocytes (n= 9) and liver (n=l) of 10 patients with anti-LKM-l antibody was analysed by Southern blot for genetic association studies between a particular CYP2D6 haplotypc and autoimmune hepatitis. In addition, a region of CYP2D6. from the same genomic DNA. was amplified by polymcrasc chain reaction (PCR) and digested by BstNI, in a search for the most prevalent 29B mutation, described in subjects who do not express the P45O IID6. Total RNA and proteins, prepared from the liver of an anti-LKM-l+ patient, were analysed by Northern and Western (immunoblot) blots respectively. Our results do not reveal any major structural change in the DNA of this patient at the CYP2D6 locus that could explain their autoimmune response. Corroborating this observation, no changes were noted either in P450 IID6 mRNA size or in the corresponding protein. However, these data do not exclude the possibility of subtle changes in the protein due to point mutations in critical regions that might trigger an autoimmune response.
Antigenic specificity and subset analysis of T cells isolated from the bronchoalveolar lavage and pleural effusion of patients with lung disease
Authors: FAITH A , SCHELLENBERG D M , REES A D M , MITCHELL D M 
Published: July 2010

SUMMARYCellular infiltraicsofbronchoalvcolarlavage(BAL)andpleuralcffusion from patients with tuberculosis (TB) and lung cancer were characterized for the presence of different T cell subsets by phenotypic analysis. The specificity of ihe T cells for mycobacierial antigens was then compared for the two disease compartments. The composition ofT cell subsets within the BAL. in contrast to pleural effusion cells (PEC), revealedevidenceofsequestrationofCD8’ cells. BALTcellswerefoundtobeapredominantly CD29’ DR’ memory population ofactivatcd cells. Although polyclonal populations of BAL T cells proliferated poorly to Mycohacterium tuberculosis antigens, mycobacierial antigen-reactive monoclonal T cell populations could be derived from the alveolar compartment. Two clones were shown to recognize the 65-kD heat shock protein of mycobactcria. and one of these clones recognized a conserved sequence of the molecule. Several BAL-derivcd clones, responding to a mycobacterial soluble extract, did not. however, recognize purified mycobacterial antigens, previously identified as highly stimulatory for PEC-derivcd T cells. T cell clones, derived from PEC of two TB patients, responded to the 38-kD and 71-kD. as well as the 65-kD mycobacterial antigens. Examination of the activation requirements of BAL-derivcd T cell clones, specific for mycobacterial antigens, revealed that exogenous IL-2 was necessary for the T cells to sustain proliferation. This was in contrast to the mycobacterial antigen-reactive T cells cloned from PEC. These results suggest that T cell populations with distinct antigen specificities and activation requirements arc present in BAL and PEC.
HBsAg in urine: a new approach for the detection of urinary antigens
Authors: BADUR S , GRANGEOT-KEROS L , PILLOT J 
Published: July 2010

SUMMARYIn order to define the optimal conditions for detection of microbial antigens in urine, urinary HBsAg excreted during hepatitis B was chosen as a model. Using commercial kits, which mainly involve anti-discontinuous epitopes, we found urinary HBsAg in only 50% of patients with HBsAg in their sera. In contrast, with an inhibition method involving a monoclonal antibody recognizing a continuous epitope, urinary HBsAg was found in 100% of these patients. Structural analysis of HBsAg showed that urinary HBsAg is denatured; it can escape detection by commercial kits well fitted for detection of native serum HBsAg. General implications for the revelation of urinary microbial antigens are discussed.