bluuebunny/crossref_metadata_2025_split huggingface dataset:
The ABA-1 allergen of the nematodeAscaris suum: epitope stability, mass spectrometry, and N-terminal sequence comparison with its homologue inToxocara canis
Authors: CHRISTIE J F , DUNBAR B , KENNEDY M W 
Published: July 2010

SUMMARYABA-1 is a major allergen of nematode parasites of the genus Ascaris which includes the large roundworms of humans and pigs, A. lumbricoides and A. suum, respectively. The allergen was purified from A. suum by immunoaffinity chromatography for immunochemical examination. The IgE antibody repertoire is under MHC control in infected rodents and the IgE-binding epitopes were robust to treatment with heat or periodate, and electroblotting on nitrocellulose. This implies that the IgE epitopes comprise primary peptide sequence or an unusually stable secondary or tertiary structure. The molecular mass of ABA-1 is controversial, but mass spectrometry analysis indicated that there were five components of similar size, with the major species being 14 643·2 ± 1·4D. Finally, N-terminal sequence analysis of ABA-1 and TBA-1 (the homologue in the canine nematode infective to humans, Toxocara canis) revealed a high degree of similarity, and we have previous evidence that ABA-1 homologues are widespread amongst ascaridid parasites of humans. ABA-1 and its homologues might, therefore, be important to the immunopathology of many infections with nematode parasites, upon which the genetic constitution of the hosts will also have a bearing.
Abnormalities of the IgA immune system in members of unrelated pedigrees from patients with IgA nephropathy
Authors: SCHENA F P , SCIVITTARO V , RANIERI E , SINICO R , BENUZZI S , DI CILLO M , AVENTAGGIATO L 
Published: July 2010

SUMMARYIn the last few years many investigators have reported the recurrence of primary IgA nephropathy (IgAN) or the presence of persistent microhaematuria and/or proteinuria in family members of patients with IgAN. Our study was undertaken to investigate the relevance of abnormalities in the regulation of the IgA and IgM immune system in microhacmaturic and asymptomatic family members of IgAN patients. Fifty-four out of 120 members of nine unrelated pedigrees were examined by urinalysis; polymeric IgA (pIgA). IgA rheumatoid factor (IgARF), IgAI-IgG immune complexes (IgAl-IgG IC) and IgAl-IgM IC, and other immunoglobulins were measured in serum samples. Moreover, we studied the production of immunoglobulins. pIgA and IgARF by peripheral blood mononuclear cells (PBMC) in basal conditions and after pokeweed mitogen (PWM) stimulation. Our data demonstrate that persistent mierohaematuria was present in 24% of relatives. High serum levels of IgA. mainly pIgA and IgARF, IgAI-IgG IC and IgAl-IgM IC occurred in 66% of relatives. Abnormal spontaneous production of IgA by PBMC and after PWM stimulation was present in 64% of family members. Interestingly, high scrum levels of IgM and abnormal production of this immunoglobulin by PBMC were observed in relatives. However, the immunological abnormalities did not correlate in any way with the presence of urinary abnormalities such as microhaematuria. which was most likely determined by an underlying glomerular alteration.
Augmentation by transferrin of IL-2-inducible killer activity and perform production of human CD8+ T cells
Authors: NAKAMURA A , SONE S , NABIOULLIN R , SUGIHARA K , MUNEKATA M , NISHIOKA Y , NII A , OGURA T 
Published: July 2010

SUMMARYThe effects of human transferrin (Tf) on lymphokine (IL-2)-activated killer (LAK) induction from blood lymphocytes of healthy donors was examined. LAK cells were induced by 6-day incubation in medium with recombinant human IL-2 of lymphocytes, and their cytotoxic activity was assessed by measuring 51Cr release from NK-resistant Daudi cells. Tf alone did not induce any LAK activity, but in combination with IL-2, it augmented LAK induction dose- and time-dependently. This augmenting effect was completely abolished by pretreatmenl with anti-Tf antiserum. Tf augmented the proliferative response of lymphocytes to IL-2 and their expressions of receptors for IL-2 and Tf. CD8+ T cells were isolated from purified blood lymphocytes using antibody-bound magnetic beads. Addition of Tf to cultures of CDS+ cells resulted in significant augmentation of killer cell induction and perforin (PFP) production after 4 days stimulation with IL-2. These results indicate that Tf is important in generation of IL-2-inducible killer properties and PFP activity of human CD8+ T cells.
The functional affinities of antibodies of different IgG subclasses to dietary antigens in mothers and their babies
Authors: DEVEY M E , BECKMAN S , KEMENY D M 
Published: July 2010

SUMMARYThe quantity and functional affinities of IgG1 and IgG4 antibodies to the dietary antigens casein and ovalbumin were measured in unselccted mothers and their 1-year-old infants. In these infants, the titre of IgG antibodies to both antigens was highest in the IgG1 subclass, while in their mothers the litre of IgG1 and IgG4 antibodies to these foods was similar. High affinity IgG4 responses to both casein and ovalbumin were frequently found in mothers, whilst IgG1 responses, particularly to ovalbumin. were of 1ow functional affinity. By contrast, in the 1-year-old infants, the functional affinity of IgG1 antibody to ovalbumin was substantially higher than in their mothers (Student's paired t-test, P &lt; 0·001). indicating that higher affinity IgG1 antibody was produced on first exposure to ovalbumin rather than following chronic exposure. The effect of antigenic load on affinity maturation was further investigated by comparing the affinity of IgG1 antibody to casein in bottle, mixed and breast fed infants. Bottle fed infants had significantly higher-affinity IgG1 antibodies to casein compared with breast or mixed fed infants (Student's unpaired t-test. P &lt; 0·01 and 0·02), suggesting that antigen exposure via the gut was able to drive the affinity maturation process. In studying the immune response it is clear that account must be taken of the affinity as well as of the litre of the antibody produced.
Regulation of resistance against adjuvant arthritis in the Fisher rat
Authors: van de LANGERIJT A G M , van LENT P L E M , HERMUS A R M M , van de PUTTE L B A , van den BERG W B 
Published: July 2010

SUMMARYInbred female Lewis (LEW/N) rats develop a severe chronic arthritis in the adjuvant arthritis (AA) model, histocompatible Fisher(F344/N) rats are resistant and germ-free Fishers (GF F344) are again susceptible. In this study we show that the F344 rat can become susceptible to AA, using Mycobavterium tuberculosis (M.tb.) in the powerful adjuvant paraffin oil, instead of mineral oil (Freund's incomplete adjuvant (FIA)). This indicates that the F344 rat does nol lack T effector cells. To examine further mechanisms responsible for suppression, we determined the level of plasma eorticosterone in response to IL-1α in Lewis. F344 and GF F344 rats. IL-lα induced only low amounts of corticosterone in Lewis rats, but high amounts in both F344and GF F344 rats. The GF F344 rats are susceptible lo AA. but the severity of the disease is redueed compared with Lewis rats. This indicates that corticosterone may be an important mechanism lo suppress disease development, but not the only mechanism. In addition we investigated whether T suppressor cells play a role in the resistance of the F344 strain. This was performed by pretreating the animals with the immunomodu-laling drugs cyelophosphamide (Cy) and cyclosporin A (CsA). We were unable to make the F344 rat susceptible to AA, indicating that active suppression does nol play a role in the induction phase of arthritis. This finding is confirmed in adoptive transfer experiments of AA from Lewis to F344 rats. Our dala suggest the lack of a strong pre-existing suppression in the F344 rats, and indicate that suppression is generated upon bacterial challenge. Whether suppression is overruled probably depends on the power of adjuvants used and potential control by corticosteroids.
Immunohistochemical demonstration of membrane cofactor protein (MCP) of complement in normal and diseased kidney tissues
Authors: ENDOH M , YAMASHINA M , OHI H , FUNAHASHI K , IKUNO T , YASUGI T , ATKINSON J P , OKADA H 
Published: July 2010

SUMMARYThe immunohistochemically stained membrane cofactor protein of complement (MCP/CD46), one of the complement regulatory proteins, was up-regulated in some diseased kidney tissues. MCP in diseased kidneys was strongly concentrated along the glomerular capillary walls as well as In the mesangial regions, while MCP in normal kidneys was weakly detected in all glomerular structural cells and in the epithelial cells of tubules. Since the enhanced staining was noted in those areas where depositions of C3b/C3c occurred, ongoing complement reaction might be responsible for the up regulation of MCP expression. MCP expression may be up-regulated by complement fragments generated during complemenl activation in glomerulonephritis. Furthermore, anti-MCP staining was stronger in intensity in patients with moderate to massive proteinuria, indicating that up regulation of MCP expression could be directly correlated to the kidney damage.
Population study of T cell receptor Vβ gene usage in peripheral blood lymphocytes: differences in ethnic groups
Authors: GEURSEN A , SKINNER M A , TOWNSEND L A , PERKO L K , FARMILOE S J , PEAKE J S , SIMPSON I J , FRASER J D , TAN P L J 
Published: July 2010

SUMMARYThe T ceil receptor (TCR) Vβ repertoire in peripheral biood lymphocytes (PBL) of a largc number of healthy individuals was analysed by quantifying Vβ-specific mRNA using the method of anchored muitiprimer DNA ampiification and a reverse dot blot assay. Among 16 Vβ gene families examined, particular Vβ genes were noted to be unequally expressed in the PBL of 70 healthy donors. The frequently used genes belong to the Vβ 4, 5, 6, 8 and 13 (12) families, while Vβ 1, 9 and 15 were the least frequently used gene families. This bias in gene usage was observed in all individuals. Marked deviation from the mean percentage usage was noted for some Vβ genes in individuals when their PBL were examined serially. but the common pattern of biased usage was not grossly distorted. When the TCR repertoire of different ethnic groups was examined, a lower mean frequency of Vβ 3·2 was seen in the repertoire of 19 Caucasians compared with 25 age-matched Samoans (P&lt; 0·003). Conversely, the expression of Vβ 5·1 and of Vβ 5·3 was higher in Caucasians than in 5 age-matchcd Polynesians (Maoris and Samoans, P&lt; 0·003). Considering the 20% co-efficicnt of variation in the estimate of Vβ gene usage, our data from 70 unrelated individuals suggest that in PBL, individual variations in the TCR repertoire were superimposed upon a common biased usage of Vβ genes in the general population.
Effects of activin A on IgE synthesis and cytokine production by human peripheral mononuclear cells
Authors: YAMASHITA N , NAKAJIMA T , TAKAHASHI H , KANEOKA H , MIZUSHIMA Y , SAKANE T 
Published: July 2010

SUMMARYActivin A not only stimulates the synthesis and release of pituitary follicle-stimulating hormone, but exerts various effects on haematopoietic cells. embryos, and fibroblasts. In the present study we have examined effects of activin A on lgE synthesis and cytokine production by peripheral blood mononuclear cells (PBMC) in normal humans. When PBMC were cultured in the presence of IL -4, activin A significantiy augmented IgE production induced by IL-4. Activin A did not affect, however, IgE production from highly purified B cells when they were stimulated with anti-CD40 MoAb and IL-4. The fact that in the latter condition IgE synthesis was T cells- and monocyte-indcpcndent indicated that activin A does not directly influence B cells for IgE synthesis. Rather, production as well as gene expression of IL-6, which is known to enhance IgE synthesis by purified monoeytes, was induced by activin A alone. In addition, activin A induced other monokines such as IL-l and tumour necrosis factor (TNF)-α from monocytes. In contrast, activin A neither induced nor augmented the production of TNF-β or interferon-gamma (IFN-γ), both of which are known to be exclusively generated by T cells. These data indicate that activin A plays a certain role in physiological functions for monocytes in normal humans.
Trypanosoma cruziinfection enhances polyreactive antibody response in an acute case of human Chagas' disease
Authors: GRAUERT M R , HOUDAYER M , HONTEBEYRIE-JOSKOWCIZ M 
Published: July 2010

SUMMARYThe kinetics of antibody response in an acute case of human Chagas' disease was investigated. Hypergammaglubulinaemia appeared at day 17 of infection, and persisted after 66 days of infection, at which time parasitaemia became undetectable. Titration of immunoglobulins showed that the three principal isotypes were involved in the response, emphasizing polyclonal B cell activation. Total IgA was detected before total IgM, and the killer before total IgG. High titres of autoantibodies were found among IgM and IgG subclasses. IgA was also the first isotype to be detected among specific anti-Trypanosoma cruzi antibodies. However, the maximal parasite antibody response was attained after 30 days of infection for all isotypes. With regard to possible cross-reactivity between molecules of host and parasite, adsorption experiments on T. cruzi-specific immunosorbent were designed. Specific antibodies, present in the eluates, also recognized natural antigens, especially laminin. In order to characterize the α-galactose epitope of laminin, adsorption experiments on sheep erythrocytes were performed, and revealed the possible presence of another epitope on the glycoprotein. Our results indicate that in the case of Chagas' disease investigated here, polyclonal activation occurred; moreover, they suggest that molecular mimicry may play a role by increasing autoantibodies, probably via a parasite-driven mechanism.
Increased IFN-α-induced sensitivity but reduced reactivity of 2′,5′-oligoadenylate synthetase (2,5AS) in trisomy 21 blood lymphocytes
Authors: GERDES A-M , HØRDER M , BONNEVIE-NIELSEN V 
Published: July 2010

SUMMARY
2,5 AS is induced by interferon-alpha, -beta (IFN-α, -β) and polymerizes adenosine triphosphate (ATP) into pppA (2′ p5′ A) oligomers, leading to inhibition of protein synthesis and virus growth. The gene coding for the IFN-α, -β receptor is localized lo chromosome 21. In trisomy 21 cells from patients with Down's syndrome a 50% increase in gene dosage is present for the genes on this chromosome. Corresponding increase of gene products has been shown for several of these genes, e.g. The IFN-α, -β receptor molecules. Here, we show a direct proportionality between the number of IFN-α, -β receptors and both the basal activity of 2,5AS and the sensitivity of this enzyme for IFN-α, -β. The relative increase of 2,5AS activity (the reactivity) becomes reduced consistent with the increased basal 2,5AS activity in trisomy 21 cells compared with control cells.
Human colonic intraepithelial lymphocytes from patients with inflammatory bowel disease fail to down-regulate proliferative responses of primed allogeneic peripheral blood mononuclear cells after rechallenge with antigens
Authors: DALTON H R , DIPAOLO M C , SACHDEV G K , CROTTY B , HOANG P , JEWELL D P 
Published: July 2010

SUMMARY
Human colonic intraepithelial lymphocytes from control subjects down-regulate the proliferative responses of primed allogeneic peripheral blood mononuclear cells on rechallenge with antigens or phytohaemagglutinin (PHA). In contrast, human colonic intraepithelial lymphocytes from patients with inflammatory bowel disease fail to down-regulate the proliferative responses of primed allogeneic peripheral blood mononuclear cells on rechallenge with antigens. These findings may be important in the development and maintenance of the mucosal immunological activation of inflammatory bowel disease.
Expression of types I, III and IV collagen genes in fibrotic skin and nerve lesions of toxic oil syndrome patients
Authors: GOMEZ-REINO J J , SANDBERG M , CARREIRA P E , VUORIO E 
Published: July 2010

SUMMARY
We have studied the skin and nerve fibrosis in toxic oil syndrome by in situ hybridization using specific cDNA probes for types I, III, and IV collagens, Fibroblasts with high levels of type I and III collagen mRNA were observed in biopsies from fibrotic skin areas. Similarly, type IV collagen mRNA was abundant in cells within the fibrotic process of the nerves. These results suggest that the excessive accumulation of collagen in toxic oil syndrome results from transcriptional activation of collagen genes in a subpopulation of fibroblasts.
Partial prevention of active Heymann nephritis by 1α, 25 dihydroxyvitamin D3
Authors: BRANISTEANU D D , LEENAERTS P , van DAMME B , BOUILLON R 
Published: July 2010

SUMMARYThe hormone 1α, 25 dihydroxyvitamin D3 (1,25(OH)2DO3 has potent immunosuppressivc effects in vitro. Recent publications also described a protective effect of the hormone in various animal models of immune-mediated diseases. To test its in vitro activity we induced active Heymann nephritis in Lewis rats that were either untreated or treated with 1,25(OH)2D3 or its synthetic 20-epi analogue, KH1060. Treatment with cyclosporine A (CsA) was used as an immunosuppressive control. In this nephrotic model the administration of 1,25(OH)2D3 (0.5 μg/kg body weight) given on alternate days during the first 13 days after active immunization significantly reduced the proteinuria as measured by weeks 7–9. This reduction was comparable to the reduction observed in rats treated with CsA (20 mg/kg) on alternate days. A second series of experiments with 1,25(OH)2D3 confirmed these findings. The level of autoantibodies was found to be significantly suppressed during the treatment time in the CsA (20 mg/kg) group, whereas the limit of significance (P=0.06) was reached in the 1,25(OH)2D3 groups that developed less proteinuria. The administration of 1,25(OH)2D3 transiently increased the mean serum calcium Concentration with 2.5 mg/dl above the pretreatmcnt values, and the urinary calcium excretion by a factor of 3–5 during the short treatment time. Treatment with the analogue KH 1060 did not reduce the proteinuria significantly. Our experiments add evidence to the hypothesis that 1,25(OH)2D3 in pharmacological doses has immunosupprcssive potency.
Adjuvant arthritis is associated with changes in the glycosylation of serum IgG1 and IgG2b
Authors: YAGEV H , FRENKEL A , COHEN I R , FRIEDMAN A 
Published: July 2010

SUMMARYThe increased amounts of agalactosyl IgG (N-linked oligosaccharides terminating with N-acetylglucoseamine (GlcNAe) in the serum of patients with rheumatoid arthritis (RA) and other chronic inflammatory diseases have suggested that agalactosyl IgG may be involved in the pathogenesis of RA. We have now evaluated the incidence of agalactosyl IgG in the Lewis rat during the course of adjuvant arthritis (AA). The modification in glycosylation of IgG was measured by means of polyclonal and monoclonal anti GlcNAe antibodies as well as by the lectin concanavalin A (Con A). The results show that Lewis rats undergo a change in serum IgG glycosylation during the course of AA. As in human RA patients, rats with AA lack terminal galactose on igG heavy chain oligosaccharides, and the terminal GlcNAe or mannose residues arc thus exposed. The degree of agalactosyl IgG was positively correlated with the incidence of disease, peaked 20 days after disease induction, and the igG gradually reverted to the fully glycosylated form thereafter. The post-arthritic glycosylation profile was very similar to that characteristic of the naive animal- Purified IgG was shown to contain two IgG subclasses, IgGI and IgG2b. which underwent changes in glycosylation. Western blot analysis revealed that IgGl expressed a higher degree of terminal mannose, whereas IgG2b expressed a higher degree of terminal GleN.Ac, These findings raise the question of the possible involvement of agalactosyl igG in immune complex-mediated inflammation.
Extracts of wheat gluten activate complement via the alternative pathway
Authors: UNSWORTH D J , WÜRZNER R , BROWN D L , LACHMANN P J 
Published: July 2010

SUMMARYWe studied the ability of wheat gluten and its subfractions to activate complement directly. A sensitive sandwich ELISA employing a monoclonal antibody (MoAb) to a C9 neoepitope exposed in the terminal complement complex (TCC), a functional haemolytic assay for C5b6 generation, and LaurelFs electrophoretic method of estimating C3 conversion to C3bi were used. On a weight-for-weight basis, enzyme solubilized Frazer's fraction three of gluten (Fill) produced approximately 75% of the complement activation seen with the potent activator zymosan. By contrast, activation with whole insoluble undigested gluten was very weak and similar to that seen with ovalbumin or β-lactoglobulin. The results were the same using normal human serum or sera from patients with coeliac disease, dermatitis herpetiformis, or hypogammaglobulinaemia as the complement source. Activation by both zymosan and Fill was blocked in 0.01 M EDTA, but not in 0.01 M EGTA with 0.0025 m magnesium chloride. Zymosan and Fill activated complement in a serum from a patient with an intact alternative pathway but classical pathway haemolytic activity (CH50) of zero. Preferential heat inactivation of the alternative pathway inhibited both zymosan- and Fill-induced activation. Our results confirm that Fill is a strong activator of the alternative pathway. We discuss how gluten enteropathy might be initiated by complement.
Antibody to mycobacterial 65-kD heat shock protein in commercial antisera
Authors: HAJEER A H , BERNSTEIN R M 
Published: July 2010

SUMMARYInhibition ELISA and immunoblotting were used to examine the antigenic cross-reactivity claimed to exist between mycobacterial 65-kD heat shock protein (hsp65) and human lactoferrin. Commercially available anti-lactoferrin antibodies produced using either Freund's complete (FCA) or Freund's incomplete adjuvant were tested for binding to recombinant mycobaeterial hsp65. Both antibody preparations showed reactivity with hsp65, this being greater with the antibody produced using FCA. However, we found no evidence of a cross-reaction. Lactoferrin failed to inhibit anti-hsp65 reactivity, while hsp65 itself did. Affinity purified anti-lactoferrin antibody showed no reaction with hsp65 by ELISA or immunoblotting. These data suggest that commercial anti-lactoferrin preparations are contaminated with antibodies to hsp65. A commercial anti-albumin antibody also bound to hsp65 in ELISA, so this may be a more general phenomenon.
Therapeutic advances in immunosuppression
Authors: THOMSON A W , FORRESTER J V 
Published: July 2010

SUMMARYImmunosuppressive therapy is appropriate for the prevention or reversal of allograft rejection, and for the treatment of autoimmune disorders and allergic disease. Recent advances in our understanding of the cellular and molecular mechanisms that regulate immune responses have paralleled elucidation of the modes of action of a variety of therapeutic immunosuppressive agents, both ‘old’ and new. These developments have identified potential targets for more refined and specific intervention strategies that are now being tested in the clinic.