bluuebunny/crossref_metadata_2025_split huggingface dataset:
Specificity andin vitrotransfer of the immunosuppressive effectof detergent-disrupted influenza virus vaccine
Authors: SMITH T L , JENNINGS R 
Published: July 2010

SUMMARYPrimed murine splenocytes give an in vitro antibody response to influenza whole virus vaccine(WVV), as measured by enzyme immunoassay (EIA). When subunit vaccine (SV) of cither influenzaA or influenza B virus was added to in vitro splenocyte cultures stimulated with WVV, the EIAantibody response to homologous WVV was reduced. This reduction in antibody response wasobserved when SV was prepared using zwitterionic detergent (empigen BB). non-ionic detergent(triton-X-100) or cationic detergent cetyl-trimethyl ammonium bromide (CTAB); it was found to beeffected only by SV of strains of the same virus subtype—when SVs prepared from a helerotypic(H3N2) strain, an H1N1 strain and an influenza B strain were added to splenocyte cultures in thepresence of WVV. When splenocytes from immunologically naive mice, exposed in vitro to SV, weretransferred to secondary cultures of primed splenocytes, the antibody response to WVV in thesecondary cultures was also reduced. Mechanisms that may suppress the in vitro antibody responseare discussed.
T lymphocyte interferon-gamma production induced byPlasmodium falciparumantigen is high in recently infected non-immune and low in immune subjects
Authors: CHIZZOLINI C , GRAU† G E , GEINOZ A , SCHRIJVERS D 
Published: July 2010

SUMMARYInterferon (IFN) alpha and gamma were measured by radio-immunoassays in supernatanls fromcultures of peripheral blood mononuclear cells (PBMC) or purified T cell subsets incubated witheither Plasmodium falciparum schizonl-enriched malaria antigen (mAg). uninfected red blood cells(RBC) or pokeweed mitogen (PWM). Cell donors were 24 clinically immune, healthy African adultnative residents of a P. falciparum-endemic region, Haut-Ogooué, Gabon, and seven non-immune. European temporary residents with a history of a single to a few malaria infections during theprevious 1 to 9 months. When PBMC were cultured in medium alone or with RBC antigen no or lowtitres of IFN-γ were detected. PBMC proliferation and IFN-γ production observed in the presence ofmAg were dose dependent and significantly correlated. When cultured with mAg. PBMC from non-immune Europeans produced significantly higher levels of IFN-γ than did PBMC from clinicallyimmune Africans. No such difference was found when PBMC were cultured with PWM. The mAg-induced IFN-γ production was due mainly to CD4+ T cells and was not enhanced by CDS+ T celldepletion. No IFN-α was detected in culture supernatants. Thus. P. falciparum antigens are able toinduce in vitro production of IFN-γ by CD4+ Tcells; however, in this sample, individuals consideredlo be clinically resistant to malaria were low producers of IFN-γ.
Stimulation of FACS-analysed CD4+ and CD8+ human tumour-infiltrating lymphocytes with ionomycin + phorbol-12, 13-dibutyrate does not overcome their proliferative deficit
Authors: STOECK M , MIESCHER S , QIAO L , CAPASSO P , BARRAS C , VON FLIEDNER V 
Published: July 2010

SUMMARYHuman tumour-infiltrating lymphocytes (TIL) were prepared by enzyme digestion from a series of different tumours and were purified on a fluorescence-activated cell sorter (FACS II) according to their CD4+ and CD8+ phenotype. CD4+ and CD8+ TIL were stimulated separately in a low density microculture system with phytohacmagglutinin (PHA) or with ionomycin plus phorbol-12, 13-dibutyrate (PDBu). The PHA-induced proliferation of TIL was highly decreased when compared with control peripheral blood lymphocytes. A decreased proliferation of TIL was also observed when cells were stimulated with ionomycin plus PDBu, a combination which is thought to circumvent early events associated with lymphocyte activation. Some TIL were also plated in limiting dilution where they showed decreased frequencies of proliferating T cell precursors. The data suggest that one component of the inhibition of TIL must be acting ‘ownstream’ of the early events of lymphocyte activation.
Reduction of graft-versus-host disease in neonatal Fl hybrid mice
Authors: DEGIORGI L , HABESHAW J A , POVEY S , MATOSSIAN-ROGERS A 
Published: July 2010

SUMMARYPre-immunization of BALB/c (H-2d) mothers with C57BL/10 (H-2b) or CBA/H (H-2k) spleen cellspartially protected the Fl hybrid offspring of (BALB/c × C57BL/10) or (BALB/c × CBA/H) matingsfrom graft-versis-host-disease (GVHD) induced by neonatal intraperitoneal inoculation with spleencells of the paternal strain. The effects achieved were manifest as a reduction in mortality. Experiments to establish whether the phenomenon was antibody mediated were performed bypassive pre-immunization of BALB/c mothers with alloantisera obtained from BALB/c previouslyimmunized with C57BL/10 spleen cells. Alloantisera produced an equivalent reduction in GVHDmortality. Some of the F1 mice that survived challenge with paternal strain spleen cells were proven tobe haemopoietic chimaeras using immunofluorescence with anti-MHC monoclonal antibodies andpolymorphism of the enzyme glucose-phosphale-isomerase present in the strains used. The possiblemechanisms of protection from GVHD in our mouse model are discussed.
The level of mannan-binding protein regulates the binding of complement-derived opsonins to mannan and zymosan at low serum concentrations
Authors: SUPER M , LEVINSKY R J , TURNER M W 
Published: July 2010

SUMMARY
When sera diluted to 5% in a buffer containing calcium and magnesium were incubated with mannancoated ELISA plates, C4 fragments, properdin and factor B were bound to the plates as well as the expected opsonic C3 fragments, C3b and C3bi. The calcium-dependent lectin mannan-binding protein, which is structurally similar to C1q, was also shown to bind in this assay and analysis of sera from 179 healthy blood donors revealed that the binding levels of all these proteins were highly significantly correlated. Results obtained with a previously described C3b opsonic assay using zymosan also correlated with the mannan-binding levels. When the sera were diluted to 5% in the presence of Mg-EGTA there was no detectable binding of complement proteins to the mannan surface, confirming that no alternative pathway activation occurred at this serum concentration. When sera were diluted to 5% in a buffer containing EDTA in order to study immunoglobulin binding in the absence of complement activation, the levels of bound IgG1, IgG2, IgG3, IgA and IgM antibodies were found to be completely unrelated to the C3bi binding levels previously observed. The results suggest that in this experimental system using low concentrations of serum, mannan-binding protein initiates an antibody-independent mechanism of cleavage of the classical pathway component C4, which subsequently regulates the degree of cleavage of C3 and recruitment of alternative pathway proteins.
Differences between C4A and C4B in the handling of immune complexes: the enhancement of CR1 binding is more important than the inhibition of immunoprecipitation
Authors: GATENBY P A , BARBOSA J E , LACHMANN P J 
Published: July 2010

SUMMARYThere are two isotypes of C4—C4A and C4B—, encoded within the major histocompatibility complex with quite different properties. In this study we have compared purified C4A and C4B with regard to their ability to prevent immune complex precipitation and to enhance the binding of both preformed and nascent immune complexes to the receptor CR1 on red cells. C4A was modestly more effective than C4B at inhibiting immunoprecipitation, particularly in antibody excess. In the CRI binding assay C4A was markedly more effective than C4B in enhancing binding to CRI. This difference was seen with both preformed and nascent immune complexes at equivalence and antibody excess. Thus the major differences between C4A and C4B in regard to immune complex handling is at the level of CRI binding. Given the strong association of C4A* QO alleles with immune complexmediated diseases like systemic lupus erythematosus, these findings have important pathogenetic implications.
Depressed degranulation response of synovial fluid polymorphonuclear leucocytes from patients with rheumatoid arthritis to IgG aggregates
Authors: DULARAY B , DIEPPE P A , ELSON C J 
Published: July 2010

SUMMARYNo difference was found between the degranulation responses to FMLP of synovial fluid (SF) polymorphonuclear leucocytes (PMNL), from patients with rheumatoid arthritis (RA), and either paired blood PMNL or blood PMNL from a healthy donor. In contrast, the response of SF PMNL to heat-aggregated IgG was often reduced compared with autologous blood PMNL. Similarly, SF from some (35%) RA patients stimulated degranulation of PMNL but the response of SF-derived PMNL to autologous stimulatory SF was reduced compared with the response of blood PMNL. The stimulatory activity of the SF was removed by sepharose-protein A. These results were taken to suggest that the activity is due to immunoglobulin aggregates and that SF PMNL (from some RA patients) are tachyphylactic to stimulation by immunoglobulin aggregates as measured by degranulation because they have been stimulated by immunoglobulin aggregates in vivo. In other studies the concentration of myeloperoxidase (MPO) was measured enzymically in RA SF and was found to be present in varying amounts. However, only a weak relationship was found between MPO levels and either PMNL numbers or levels of complement-bearing IgG aggregates in SF. It is considered that the relationship between MPO and immunoglobulin aggregates levels is obscured by the presence of a peroxidase inhibitor in the fluids and/or because only aggregates bound to tissue stimulate degranulation in vivo.
Adsorption of anti-dsDNA antibodies by immobilized polyanionic compounds
Authors: AOTSUKA S , FUNAHASHI T , TANI N , OKAWA-TAKATSUJI M , KINOSHITA M , YOKOHARI R 
Published: July 2010

SUMMARY
Antibodies to dsDNA are characteristically present in serum from patients with systemic lupus erythematosus (SLE). and have been shown to have the capacity to react with various molecules bearing repeating negative charges. After a number of polymeric or monomeric molecules with differently charged groups and hydrophobic molecules had been coupled covalently as ligands on cellulose gel, the adsorption capacities of the ligands for anti-dsDNA antibodies were evaluated. It was found that gels coupled with polyanionic dextran sulphate (DXS) and polyacrylic acid (PA) and monoanionic sulphanilic acid (SA) absorbed anti-dsDNA antibodies effectively. DXS gel also adsorbed antibodies to ssDNA and heparan sulphate, antigens with repeating negatively charged moieties, while no ligand was able to adsorb anti-nRNP antibodies. The finding that DXS gels adsorbed anti-dsDNA antibody in proportion to their charge density, and that the interaction between anti-dsDNA and DXS gel is broken readily by an increase in ionic strength, indicated that the binding is ionic in nature. Moreover, virtually all F (ab′)2 anti-dsDN A became adsorbed onto the DXS gels, suggesting that the binding occurred via specific antigen-binding sites on the antibody molecule. Binding of these polyanion-binding autoantibodies with anionic sites in the glomerular basement membrane may therefore cause the tissue damage observed in SLE.
Quantitative study ofLeishmania braziliensis braziliensisreactive T cells in peripheral blood and in the lesions of patients with American mucocutaneous leishmaniasis
Authors: CONCEIÇÃO-SILVA F , DÓREA R C C , PIRMEZ C , SCHUBACH A , COUTINHO S G 
Published: July 2010

SUMMARYA limiting dilution analysis (LDA) was utilized to estimate the frequency of L. braziliensis braziliensis reactive T cells (Lbb-T cells) in peripheral blood and in the lesions of patients with mild localized cutaneous leishmaniasis (LCL) or with severe mucosal leishmaniasis (MCL). The frequencies of Lbb-T cells in peripheral blood varied from 1:107 300 to 1:3587 and were not significantly different in MCL and LCL patients. However, a significant difference was encountered (P &lt;0.02) between the T cells frequencies in cutaneous (1:748 to 1:45) and mucosal lesions (1:152 to 1:13). A positive correlation was also observed between these frequencies and the magnitude of delayed-type hypersensitivity (DTH) (P &lt; 0.01) and the presence of fibrinoid necrosis and granulomatous reaction in the site of the lesions (P&lt;0.05). The lack of correlation between the severity of disease (MCL or LCL) and the frequency of Lbb-T cells in peripheral blood gave no indications towards understanding the physiopathology of severe or mild disease. However, the correlation between high T cell frequencies in the site of the lesions, the magnitude of DTH, the fibrinoid necrosis and the severity of the disease (MCL lesions) points to the possibility that the presence of a strong T cell dependent cellular immune response in the site of the lesions may have a deleterious effect. However, a local well modulated T cell immune response might provide healing of the lesions.
Therapy of a fatal murine cytomegalovirus infection with thymic humoral factor (THF-γ2) treated immune spleen cells
Authors: RAGER-ZISMAN B , ZUCKERMAN F , BENHARROCH D , PECHT M , BURSTEIN Y , TRAININ N 
Published: July 2010

SUMMARYInfection of mice with murine cytomegalovirus (CMV) presents a model for the study of the role of the immune system in the pathogenesis of human CMV. We performed adoptive transfer experiments to evaluate the prospects for enhancing the anti-viral potential of murine CMV immune spleen cells by THF-γ2. Adult BALB/c mice resistant to murine CMV become highly susceptible following immunosuppression by cyclophosphamide. Recipient mice were injected with murine CMV and cyclophosphamide concomitantly, and 24 h later adoptive transfers of syngeneic immune spleen cells were performed. We showed that passive transfers of murine CMV immune spleen cells prevented the development of a fatal disease in 38% of the recipient mice. Daily injections of murine CMV immune donor mice with THF-γ2 enhanced considerably (93%) the therapeutic potential of virus-specific immune cells. These experiments provide direct evidence for the antiviral capacity of THF-γ2 through its immunomodulatory effect on immune T cells.
Flare-up reaction of streptococcal cell wall induced arthritis in Lewis and F344 rats: the role of T lymphocytes
Authors: VAN DEN BROEK M F , VAN BRUGGEN M C J , STIMPSON S A , SEVERIJNEN A J , VAN DE PUTTE L B A , VAN DEN BERG W B 
Published: July 2010

SUMMARYOne i.p. injection of a sterile suspension of streptococcal cell walls (SCW) induces chronic erosive polyarthritis in susceptible Lewis rats, but not in resistant F344 or nude Lewis rats. Because continuous exacerbations may be one possible mechanism underlying chronic disease, we studied the mechanism of these flare-up reactions in Lewis and F344 rats. Injection of SCW into the right knee joint of rats induced a transient monoarthritis in both strains. Reactivation of the subsided arthritis by i.v. administration of the same antigen could be evoked only in the Lewis rat. Even repeated i.v. challenges with SCW failed to induce a flare-up reaction in the F344 rat, while the Lewis rat went through an exacerbation after every challenge. Removal of T lymphocytes by monoclonal antibodies before induction of an exacerbation rendered Lewis rats refractory to flare-up reactions, thus indicating the T cell-dependence of this reaction. Furthermore, when cell walls from heterologous bacteria were tested for their capacity to induce exacerbations of SCW-induced monoarthritis and to induce proliferation of SCW-specific T lymphocytes in vitro, a strong correlation between both features was found, again pointing to a role for SCW-specific T cells in exacerbations. Together, these data support our hypothesis that chronic arthritis is the result from repeated reactivations of a waning arthritis which are dependent on antigen-specific T lymphocytes.
Activation process of macrophages afterin vitrotreatment of mouse lymphocytes with dodecylglycerol
Authors: HOMMA S , YAMAMOTO N 
Published: July 2010

SUMMARYAlkylglycerols, inflammation products of cancerous membrane lipids, efficiently activate macrophages. A brief in vitro treatment (30 min) of peritoneal cells (mixture of non-adherent and adherent cells) with a small amount (50 ng/ml) of synthetic dodecylglycerol (DDG) resulted in greatly enhanced Fc-receptor-mediated ingestion activity of macrophages. However, treatment of adherent cells (macrophages) alone with DDG produced no significant enhancement of macrophage ingestion activity, implying that macrophage activation requires a contribution of non-adherent cells. DDG-treated non-adherent cells were found to generate a macrophage-activating signal factor. Studies with a serum free-0.1 % egg albumin-supplemented RPMI 1640 medium revealed that a serum factor is essential for macrophage activation process. Time course analysis of stepwise transfers of conditioned media of DDG-treated or untreated B cells and T cells revealed that DDG-treated B cells rapidly transmit a factor to untreated T cells which yield the ultimate macrophage-activating factor. This signal transmission among these cells for the macrophage activation process is too rapid to allow time for synthesis of inducible gene products. Thus, we hypothesized that a serum factor is modified by the pre-existing function of DDG-treated B cells and further modified by the pre-existing function of untreated T cells to yield macrophage-activating factor. This hypothesis was confirmed by the demonstration that DDG-treated splenic non-adherent cell ghosts modify a serum factor to yield macrophage-activating factor.
Actuarial rate of clinical and biological progression in a cohort of 250 HIV-1-seropositive subjects
Authors: VENET A , TOURANI J-M , BELDJORD K , EME D , EVEN P , ANDRIEU J-M 
Published: July 2010

SUMMARY
This study was undertaken to define the risk of AIDS in a cohort of 250 HIV-seropositivc patients identified by their clinical and biological status. All patients were enrolled between October 1985 and March 1988. They were classified according to clinical classes A, asymptomatic (n= 97); B. lymphadenopathic(n= 123); and C, AIDS-related complex, (n= 30). Also as CD4 cell stages 1 (CD4 ± 600/μl;n= 126); 2(CD4 &lt; 600 and ± 300/μ1; n= 83); and 3 (CD4 &lt; 300/μl; n= 41); and serum p24 antigen positive (n= 48) or negative (n= 202). All patients were evaluated every 3–6 months, until AIDS development or April 1989: 29 cases of AIDS occurred during the follow-up period. The risk of AIDS in class C is very high (64% at 2 years) compared with the 3-year risk of classes A (13%) and B (25%). On the other hand the three CD4 stages have significantly different prognosis (stage 1 6%; stage 2 22%; and stage 3 89%; P &lt; 10−2). Antigen p24 negative and positive patients have also different prognosis (18% and 53%; P &lt; 10−4). Interestingly. p24 antigen conserved its prognostic value in stage 2 (positive 37%. negative 16%) while stages I are at low risk of AIDS and stages 3 at high risk whatever their p24 antigen status. We have also identified the risk of becoming stage 3 and/or p24 antigen positive in p24 antigen negative patients at stages 1 and 2 (respectively, 18% and 47%). This classification should serve to design randomized trials better with experimental drugs with earlier end-points than AIDS onset.
Alveolar macrophages in AIDS patients: increased spontaneous tumour necrosis factor-alpha production inPneumocystis cariniipneumonia
Authors: KRISHNAN V L , MEAGER A , MITCHELL D M , PINCHING A J 
Published: July 2010

SUMMARYIn order to assess the role of alveolar macrophages and their products in the control of Pneumocystis carinii pneumonia (PCP) and other infections in AIDS, bronchoalveolar lavage cells and peripheral blood mononuclear cells from HIV-positive AIDS/ARC patients (with and without PCP) and HIV-negative patients were counted and cultured in vitro; spontaneous and LPS-induced tumour necrosis factor-alpha (TNF-α) production was measured. Markedly increased spontaneous TNF-α production by alveolar macrophages and, to a lesser extent, peripheral blood monocytes was found in HIV-positive patients with active PCP but not in patients without the infection. Higher TNF production was associated with lower counts of Pneumocystis in the bronchoalveolar lavage fluid. These results suggest that TNF-α production by macrophages may play an important role in the control of Pn. carinii infection in AIDS.
Heterogeneity of binding reactivity to different phospholipids of antibodies from patients with systemic lupus erythematosus (SLE) and with syphilis
Authors: LOIZOU S , MACKWORTH-YOUNG C G , COFINER C , WALPORT M J 
Published: July 2010

SUMMARYThe binding specificities were investigated of anti-phospholipid antibodies derived from sera from 55 patients with SLE and related diseases, and from 33 patients with syphilis. Antibodies from both these groups of patients bind strongly to cardiolipin in solid-phase immunoassays, but only anti-phospholipid antibodies from patients with autoimmune diseases are associated with thrombotic complications and recurrent spontaneous abortions. IgG anti-phospholipid antibodies from both groups of patients cross-reacted with a range of negatively charged phospholipids, but binding to neutral phospholipids was largely restricted to sera from patients with syphilis. A monoclonal IgMλ anti-cardiolipin antibody, derived from a patient with autoimmunity, was used to inhibit binding of anti-phospholipid antibodies to cardiolipin and to phosphatidic acid. This antibody inhibited the binding of autoimmune sera to cardiolipin more strongly than sera from syphilis patients, but the converse pattern of inhibition of binding to phosphatidic acid was observed. The VDRL litre correlated with anti-phospholipid antibody activity in sera from syphilis patients, but not from those with autoimmunity. Lupus anti-coagulant activity correlated weakly with IgG antibody levels to each of the negatively charged phospholipids among the patients with autoimmunity. Lupus anticoagulant activity did not correlate uniquely with any anti-phospholipid antibody specificity. These results provide further documentation of the great heterogeneity of anti-phospholipid antibodies associated with autoimmune disease and syphilis.
Reactivity of human monoclonal IgM with nerve glycosphingolipids
Authors: HAUTTECOEUR B , SCHMITT C , DUBOIS C , DANON F , BROUET J C 
Published: July 2010

SUMMARY
We examined the reactivity of monoclonal IgM of sera from patients with neuropathy and monoclonal IgM, with or without antibody activity to myelin-associated glycoprotein (MAG), as well as sera from non-neurologic patients with Waldenström's macroglobulinaemia, with various nerve glycolipids extracts or with purified gangliosides. As expected from previous studies, all (five cases) anti-MAG IgM stained two glycolipids, the chemical characteristics of which corresponded to sulphated glucuronyl-paragloboside (SGPG) and sulphated glucuronyl-lactosaminyl-paragloboside (SGLPG). Five of 12 sera from patients with neuropathy whose IgM was devoid of anti-MAG reactivity stained nerve extracts greatly enriched (98%) with SGPG and SGLPG. Three of these five sera reacted with additional glycolipids and/or gangliosides. Two of 16 sera from patients with macroglobulinaemia without neuropathy reacted strongly with both SGPG and SGLPG. The latter finding as well as the detection of low titre of anti-sphingolipid antibodies in normal sera may cast a doubt on the pathogenetic significance of this antibody activity.