bluuebunny/crossref_metadata_2025_split huggingface dataset:
Avidity of Aspergillus umbrosus IgG antibodies in farmer's lung disease
Authors: KAUKONEN K , SAVOLAINEN J , VIANDER M , TERHO E O 
Published: July 2010

SUMMARY
Farmer's lung disease (FL), the commonest form of allergic alveolitis caused by repeated inhalation of mouldy hay is associated with exposure lo the fungus Aspergillus umbrosus among Finnish farmers. The antigen-binding avidity of A. umbrosus-specific IgG antibodies was measured in 12 EL patients in acute phases of initial and recurrent attacks and during 1 year follow up as well as in 12 healthy farmers and five healthy urban controls. The farmers' groups were further divided into two subgroups: subjects with short exposure (&lt; 7 years) and subjects with long exposure (&gt; 25 years). During the first acute phase PL patients with long exposure exhibited a high avidity of A. umbrosus-specific IgG antibodies that remained high during t he 1 year follow up, although the A. umbrosus-specific IgG antibody titre decreased. A re-exposure to mouldy hay leading to a recurrence further enhanced the maturation of the antibody avidity, so that an even higher A. umvrosus-specific IgG avidity with a less significant increase of antibody titre occurred than during the first acute attack. Notably higher IgG antibody avidity was observed in FL patients with long exposure than in healthy farmers or in healthy controls.
MHC class I, MHC class II and intercellular adhesion molecule-1 (ICAM-1) expression in inflammatory myopathies
Authors: BARTOCCIONI E , GALLUCCI S , SCUDERI F , RICCI E , SERVIDEI S , BROCCOLINI A , TONALI P 
Published: July 2010

SUMMARYWe investigated the relationship between the MHC-I, MHC-II and intercellular adhesion molecule-1 (ICAM-1) expression on myofibres and the presence of inflammatory cells in muscle specimens of 18 patients with inflammatory myopathies (nine polymyositis, seven dermatomyositis, two inclusion body myositis). We observed MHC-I expression in muscle fibres, infiltrating mononuclear cells and endothelial cells in every specimen. In seven patients, some muscle fibres were MHC-II-positive for the DR antigen, while the DP and DQ antigens were absent. ICAM-1 expression, detected in seven patients, was found in clusters of myofibres, associated with a marked MHC-1 positivity and a widespread mononuclear infiltration. Most of the ICAM-1-positive fibres were regenerating fibres. Furthermore, some fibres expressed both ICAM-I and DR antigens near infiltrating cells. This finding could support the hypothesis that myofibres may themselves be the site of autosensitization.
Disturbed immunoregulatory properties of the neuropeptide substance P on lymphocyte proliferation in HIV infection
Authors: COVAS M J , PINTO L A , VICTORINO R M M 
Published: July 2010

SUMMARYThe neuropeptide substance P (SP) is known to increase cell-mediated immune responses in animal models and healthy subjects. Several studies have suggested an involvement of neuropeptides in the immunopathogenesis of some diseases. The study of the immunomodulatory effects of neuropeptides, namely SP. may represent a model for the analysis of Immunoregulatory defects in HIV infection at the level of the interaction between the immune and nervous systems, both of which are known to be affected by the virus. In the present study, we investigate the possibility of a disturbance in the immunomodulatory properties of SP in HIV infection by analysing the effects of SP (10−10 10−6) on the lymphocyte proliferative responses to concanavalin A (Con A) and phytohaemagglutinin (PHA) assessed by3H-thymidine incorporation in peripheral blood lymphocytes from 34 HIV-infected patients (16 asymptomtic (ASY) persistent generalized lymphadenopathy (PGL); 18 ARC/AIDS) and in 37 healthy subjects. In ASY/ PGL HIV-infected patients, SP 10−7M was identified as the concentration inducing the maximal increase in the lymphocyte responses to Con A and PHA, similarly to what was observed in healthy subjects. In ARC/AIDS patients, SP appeared to inhibit the mitogenic responses, particularly those induced by Con A. in contrast to the effects found either in healthy subjects or in ASY/PGL patients. These results suggest the existence of an alteration in the in vitro immunomodulatory properties of SP in ARC/AIDS patients compared with healthy subjects and ASY/PGL patients. In conclusion, the unexpected finding of an inhibitory effect of SP on lymphocyte proliferation from ARC/AIDS patients justifies further investigation of the neuropeptide-dependent immunoregulatory systems in HIV infection.
Antibody-dependent enhancement of HIV-1 infection in human term syncytiotrophoblast cells culturedin vitro
Authors: TÓTH F D , MOSBORG-PETERSEN P , KISS J , ABOAGYE-MATHIESEN G , ZDRAVKOVIC M , HAGER H , ARANYOSI J , LAMPÉ L , EBBESEN P 
Published: July 2010

SUMMARYWe examined if Fc receptor-mediated antibody-dependent enhancement (FcR-ADE) or complement-mediated antibody-dependent enhancement (C′-ADE) of virus infection can contribute to increasing replication of HIV-1 in human syncytiotrophoblast (ST) cells. Here we report that both FcR-ADE and C′-ADE may result in enhanced virus release from HIV-1-infected ST cells. We show that FcR-ADF of HIV-1 infection in ST cells is mediated by FcRIII and other FcR(s) belonging to undetermined Fc classes and does not require CD4 receptors, whereas C'-ADE uses both CD4 and CR2-like receptors. FcR-ADE: seems to be more efficient in enhancing HIV-I replication than C′-ADE. While FcR-ADE leads to increased internalization of HIV-1. C′-ADE does not result in enhanced endocytosis of the virus. In addition, antibodies mediating FcR-ADE arc reactive with the gp120 viral envelope antigen, whereas antibodies involved in C′-ADE react with the viral transmembrane glycoprotein gp41. Data suggest that both FcR-ADH and C′-ADE may contribute lo the spread of HIV-1 from mother to the fetus.
Adenovirus infection induces loss of HLA class I and CD3 antigens, but does not induce cell surface presentation of the La (SS-B) autoantigen
Authors: PEEK R , WESTPHAL J R , PRUIJN G J M , VAN DER KEMP A J W , VAN VENROOIJ W J 
Published: July 2010

SUMMARYAntibodies to the RNA polymerase III transcription termination factor La arc frequently found in the serum of patients with various autoimmune diseases. The mechanisms by which autoimmune responses are evoked remain largely obscure, hut the presentation of autoantigens on the cell surface during stress conditions has been reported as a possible factor. In this study we analysed the effects of adenovirus infection on the binding of anti-La antibodies to the surface of several human cell lines and on the levels of the membrane-expressed glycoproteins HLA class I. CD44 and (hcCD3 complex. In addition, we studied the relative amount and the intracellular distribution of the La protein as well U its association with the major species of non-coding virus-associated (VAI) RNA. While immunofluorescence patterns revealed a redistribution and possibly cell surface expression of the L a protein during infection, this could not be confirmed by other techniques. In contrast, surface levels of HLA class I proteins and CD3 complex were severely affected. The data suggest that the subcellular distribution of the La protein is not detectably influenced by adenovirus infection.
Lymphokine-activated killer cell function of peripheral blood mononuclear cells, spleen cells and regional lymph node cells in gastric cancer patients
Authors: KARIMINE N , ARINAGA S , INOUE H , NANBARA S , UEO H , AKIYOSHI T 
Published: July 2010

SUMMARYLymphokine-activated killer (LAK) cells generated by culture of peripheral blood mononuclear cells (PBMC). spleen cells (SPC) and regional lymph node cells (LNC) with IL-2 for 4 days were examined for their functional capabilities m 29 patients with gastric carcinoma. The cytotoxic activity of LAK cells induced from LNC was significantly lower than that from either PBMC or SPC. although there was no difference between PBMC or SPC. The induction of mRNA of interferon-gamma (IFN-γ) or tumour necrosis factor-alpha (TNF-α) and the production of these cytokines in the non-adherent LAK cells from LNC were also significantly reduced compared with those from PBMC or SPC. Further, the LAK cells from LNC secreted significantly lower levels of these cytokines when stimulated with tumour target, Raji cells, although the production of these cytokines was markedly increased by stimulation with the targets in all three cell populations. Phenotypic analysis of each cell population revealed a decreased proportion of the cells mediating natural killer (NK) activity, including CD16+. CD56+, and CD57+ cells in LNC either before or after culture, although OKIal+ and CD25+ cells were uniformly increased in all ceil populations after culture. Changes in subpopulations of CD4+ and CD8+ cells in LNC were not apparently different from PBMC or SPC. These results indicated the differential reactivity of each lymphocyte population to IL-2 and the reduced LAK cell function of LNC compared with PBMC or SPC in patients with gastric carcinoma.
The effects ofin vivocyclosporin A administration on rat thymic dendritic cells
Authors: DAMOISEAUX J G M C , BEIJLEVELD L J J , VAN BREDA VRIESMAN P J C 
Published: July 2010

SUMMARYCyclosporin A (CsA) induces a graft-versus-host-like disease (GVHD) in lethally irradiated Lewis rats reconstituted with syngeneic bone marrow. The role of the thymus in the generation of disease has been unequivocally established. It has been suggested that the CsA-induced disappearance of thymic dendritic cells (DC) is responsible for the generation of the autoaggressive cells. In this study we quantify the loss of DC upon in vivo CsA administration in normal and bone marrow-reconstituted rats using an isolation technique. The phenotype of the DC is determined using MoAbs recognizing antigens which are expressed on thymic medullary DC. Furthermore, the functional aspects are assessed by determining the antigen presentation capacity. Short-term CsA exposure clearly affects the number of DC isolated from the thymus in a concentration-dependent manner. However, in all instances a substantial number of DC can be isolated from CsA-treated animals. These isolated DC exhibit an identical phenotype and function as DC isolated from control animals. Therefore, the partial deficiency of DC can not be held as essential for loss of tolerance.
Age-related increase in the fraction of CD27−CD4+ T cells and IL-4 production as a feature of CD4+ T cell differentiationin vivo
Authors: NIJHUIS E W P , REMARQUE E J , HINLOOPEN B , VAN DER POUW-KRAAN T , VAN LIER R A W , LIGTHART G J , NAGELKERKEN L 
Published: July 2010

SUMMARYThe influence of ageing on phenotype and function of CD4+ T cells was studied by comparing young (19-28 years of age) and aged (75 84 years of age) donors that were selected using the SENIEUR protocol to exclude underlying disease. An age-related increase was observed in the relative number of memory cells, not only on the basis of a decreased CO45RA and increased CD45RO expression, but also on the basis of a decrease in the fraction of CD27+CD4+ T cells. Our observation that the absolute number of CD45RO+ CD4+ T cells was increased, while absolute numbers of CD27-CD4+ T cells remained unchanged in aged donors, indicates that the latter subset does not merely reflect the size of the CD45RO+ CD4+ T cell pool. The increased fraction of memory cells in the aged was functionally reflected in an increased IL-4 production and T cell proliferation, when cells were activated with the combination of anli-CD2 and anti-CD28, whereas lL-2 production was comparable between both groups. No differences were observed with respect to proliferative T cell responses or IL-2 production using plate-bound anti-CD3 or phytohaemagglutinin (PHA). The observation that IL-4 production correlated with the fraction of memory cells in young donors but not in aged donors suggests different functional characteristics of this subset in aged donors.
A human monoclonal IgA autoantibody—185/12—behaves like an autoimmune antiphospholipid antibody
Authors: YRON I , SHOHAT L , LAHAV J , WITZ I P , FISCH B 
Published: July 2010

SUMMARYA human monoclonal anticardiolipin autoantibody (ACA) of the IgA-k isotype, designated 185/ 12, is described. The antibody was prepared from peripheral B cells, obtained from a patient with a history of habitual abortion, by immortalization with Epstein Barr virus (EBV). The antibody displays a strong binding activity to cardiolipin and phosphatidyl i-serine. but not to phosphatidyicholine, phosphatidylinositol, ssDNA and dsDNA, It binds to cardiolipin in a concentration-related and saturable manner (Kd = 3·0 × 10−8 M). This reaction is dependent upon the presence of bovine serum, and is fully inhibited by cardiolipin vesicles. The 185/12 antibody exhibits different binding patterns to the solid-phase bound cardiolipin-serum complex and to its individual components (cardiolipin and bovine serum). The βmax of 185/12 binding to the complex (0·968 OD units) is higher than the sum of the βmax values calculated for each one of the complex components (0·352 + 0·179 = 0·531 OD units). Bovine serum as well as purified /Vglycoprotein I (β2-GPI) in suspension inhibit the binding of 185/12 to the complex. 185/12 binding capacity increases in direct relation to the rising concentration of/β2 -GPL Collectively, these data may be interpreted to suggest that 185/12 antibody, which is an IgA isotype. exhibits characteristics usually attributed only to antiphospholipid autoantibodies (APA) of the IgG isotype. that are associated with the clinical spectrum of APA syndrome (APA-S). It is, therefore, possible that autoantibodies of the IgA isotype could play a pathogenic role, which may be different from that of the IgG isotype. in the development of autoimmune phenomena.
CD4+ T cells from collagen-induced arthritic mice are essential to transfer arthritis into severe combined immunodeficient mice
Authors: KADOWAKI K M , MATSUNO H , TSUJI H , TUNRU I 
Published: July 2010

SUMMARYThe role of T lymphocytes in the adoptive transfer of collagen-induced arthritis (CIA) in DBA/IJ mice to severe combined immunodeficient (SCID) mice was investigated. Spleen cells from non-immunized, type I collagen (CI) or type II collagen (CII)-immunized DBA/I J mice were injected into SCID mice which lack functional T and B cells. Specific antigenic stimulation of arthritogenic cells was required since only lymphocytes from arthritic CIA mice plus simultaneous administration of CII transferred arthritis to 11 of 12 SCID mice with a marked increase in CII antibody titre. However, CI-immunized or non-immunized DBA/IJ mice cells did not induce arthritis in SCID mice, SCID recipients of pre-arthritic CIA lymphocytes presented increase in CII antibody, but showed no clinical signs of arthritis, suggesting that antibodies to CII alone can not induce CIA. Depletion of CD4+ T cells inhibited the transfer of arthritis to SCID mice, with a decrease in CII antibody titre in chimaeras. In contrast, depletion of CD8+ cells enhanced the onset of arthritis in SCID mice. The results imply that CD4+ T cells are required for the induction of CIA. In addition, CD8 + T cells might have a suppressive role in the etiology of this disease. It is probable that memory CD4+ T cells stimulate production of antibodies to CII and subsequent arthritis. This study clarifies the role of T lymphocytes in the transfer of CIA lo SCID mice.
Heat shock protein peptides reactive in patients with Behçet's disease are uveitogenic in Lewis rats
Authors: STANFORD M R , KASP E , WHISTON R , HASAN A , TODRYK S , SHINNICK T , MIZUSHIMA Y , DUMONDE D C , VAN DER ZEE R , LEHNER T 
Published: July 2010

SUMMARYMycobacterial and homologous human heat shock protein T cell peptide epitopes specific for T lymphocytes in Behçets disease were investigated for their pathogenicity in Lewis rats. The potential pathogenicity of eight peptides and two controls was assessed by administering the peptides in enriched Freund's adjuvant into the footpads of male Lewis rats. Anterior uveitis which is a major manifestation of Behçet's disease was induced with two out of the four mycobacterial and all four homologous human peptides. The most effective peptides inducing indocyclitis in 64–75% of rats were peptides with amino acids 336–351 and 136–150, derived from the sequence of the human 60-kD heat shock protein. A few of the rats also showed evidence of focal loss of photoreceptors. These results suggest that selected peptides within heat shock protein 60 kD which function as T cell epitopes in Behçet's disease are capable of inducing uveitis in rats. This supports the view that the peptide T cell determinants may be involved in the pathogenesis of Behçet's disease.
Cytokine regulation of low-affinity IgE receptor (CD23) on monocytes from asthmatic subjects
Authors: VECCHIARELLI A , SIRACUSA A , MONARI C , PIETRELLA D , RETINI C , SEVERINI C 
Published: July 2010

SUMMARYThe regulation of CD23 expression (FcεRII) by cytokines on monocytes from normal subjects, asymptomatic and acute asthmatics was investigated. CD23 was weakly expressed on cells from controls, but was significantly enhanced in the two groups of asthmatics. The addition of IL-4 on monocytes induced an increase of CD23 expression in cells from controls and asthmatics. Interferon-gamma (IFN-γ) did not modulate CD23 expression in asthmatics or control subjects, while high doses of IL-6 (2000 U/ml) enhanced CD23 expression on cells from asthmatics or controls. In vitro stimulation of monocytes with Timothy grass pollen allergen did not enhance CD23 receptor in asthmatics with a positive skin test to this pollen. We speculate that CD23 expression in asthmatics is markedly enhanced by Th2-dependent cytokines, such as IL-4 and IL-6. Thus, the regulation of Th2 cell activation by anti-cytokine therapy could have an important effect on the down-regulation of CD23 on monocytes, and in shifting a Th2 subpopulation into a Th1 subpopulation by blocking Th2-dependent cytokines.
IgE production in atopic patients is not related to IL-4 production
Authors: VAN DER POUW KRAAN C T M , AALBERSE R C , AARDEN L A 
Published: July 2010

SUMMARYTo analyse whether there is a general defect in T or B cell function in atopic individuals we have measured cytokine and IgE production by peripheral blood lymphocytes, isolated from 19 atopic donors (17 asthma/rhinitis and two dermatitis patients) in comparison with 19 non-atopic controls. After stimulation of lymphocytes with anti-CD2 and anti-CD28, we found no significant difference in IL-2, IL-4 and interferon-gamma (IEN-γ) production. To examine the correlation between the production of IgE and IL-4, we stimulated lymphocytes with anti-CD2 and rIL-2. Under this condition both T cell IL-4 and B cell IgE production can be measured. No significant difference was found for the amount of IgE and IL-4 produced between the two groups (P &gt; 0·05). The non-atopic donors showed a good correlation between IL-4 and IgE production (r= 0·70). Surprisingly, within the atopic group there was no correlation between IgE and IL-4 production at all (r= −0·04). The ratio of IgE to IL-4 was higher (although not significantly) in the atopic group. Our data suggest that in atopic donors IgE production is less dependent on IL-4, and that other cytokines are involved.
Multispecific and heterogeneous recognition of the gag protein by cytotoxic T lymphocytes (CTL) from HIV-infected patients: factors other than the MHC control the epitopic specificities
Authors: BUSEYNE F , JANVIER G , ELEURY B , SCHMIDT D , RIVIÈRE Y 
Published: July 2010

SUMMARYThe HIV gag polyprotein is a major target for recognition by CTL in infected humans. Using recombinant vaccinia viruses (rVV) expressing truncations of the p24gag, and the p18gag, p15gagand HIV-2 p56gag proteins, the characterization of epitope regions recognized by in vitro-stimulated peripheral blood mononuclear ceils (PBMC) from 18 infected patients has been studied. The gag-specific response of most individuals is polyclonal and multispecific, and inter-individual variations between target epitope regions were frequently observed, despite shared MHC alleles. As CTL may play an important role in the control of HIV replication in infected hosts, these results have important implications for designing vaccine strategies.
Cytokines in nasopharyngeal secretions; evidence for defective IL-1β production in children with recurrent episodes of acute otitis media
Authors: LINDBERG K , RYNNEL-DAGÖÖ B , SUNDQVIST K-G 
Published: July 2010

SUMMARY
The host-parasite relationship in the nasopharynx of young children with bacterial colonization and antigen uptake in the mucosa and lymphatic tissue provides an opportunity to investigate infectious inflammatory processes and responses. IL-1β, IL-6 and tumour necrosis factor-alpha (TNF-α) were analysed in nasopharyngeal secretions and serum from children with or without recurrent episodes of acute otitis media, from healthy adults and adults with hypogamma-globulinaemia or selective deficiency of IgG3. Nasopharyngeal secretions generally contained substantial amounts of IL-1β, IL-6 and TNF-α. In contrast. IL-1β, IL-6 and TNF-α were not detectable in sera on the same occasion. Children were found to have higher levels of IL-1β, IL-6 and TNF-α than healthy adults and than adults with immunodeficiency. High levels of IL-IJ were associated with low or undetectable levels of IL-6 and TNF-α, whereas the opposite pattern was seen in association with low levels of IL-lβ This was especially true for children with recurrent episodes of acute otitis media (RAOM). In children with nasopharyngeal colonization with Haemophilus influenzae, significantly higher levels of IL-1β, IL-6 and TNF-α (P = 00001. respectively) were found compared with non-colonized children. Notably, the RAOM children exhibited significantly lower levels of IL-1β IL-6, and TNF-α in nasopharyngeal secretions (P = 00001, 0.01 and 0.0001, respectively) than healthy children. These results demonstrate local production of inflammatory cytokines in nasopharynx, related to bacterial colonization, and suggest that children with RAOM are poor nasopharyngeal cytokine producers.
IL-1α gene expression and protein production by fibroblasts from patients with systemic sclerosis
Authors: KAWAGUCHI Y 
Published: July 2010

SUMMARYWe examined IL-1α and IL-1β gene expression and protein production in human dermal fibroblasts from patients with systemic sclerosis (SSc) to investigate the abnormal function of SSc fibroblasts. Human dermal fibroblasts were biopsied from 13 patients with SSc. three patients with rheumatoid arthritis (RA) and five healthy normal controls (NC). Cells were cultured in serum-free media and total RNA was collected from second or third passage fibroblasts. In cultured SSc fibroblasts. IL-1α and IL-1β mRNAs were constitutively expressed and intracellular pro-IL-1α was present. These observations suggest that an autocrine effect of IL-1α contributes to the fibrosis in SSc.