bluuebunny/crossref_metadata_2025_split huggingface dataset:
Phenotypical and functional evaluation of CD8+/S6F1+ T lymphocytes in haemophiliac individuals with HIV-1 infection
Authors: CAVALLIN F , TRALDI A , ZAMBELLO R 
Published: July 2010

SUMMARYIn this study we investigated the distribution of the S6F1 antigen, an epitope of the lymphocyte function-associated antigen, on CD8+ T lymphocytes in a series of 15 HIV-1+ and 20 HIV-1- haemophiliac patients. MoAbs recognizing the S6K1 antigen have been claimed to distinguish between killer electors (brightly S6F1+ stained) and suppressor cells (dimly S6K1+ stained) within the CD8+ lymphoid population. In addition, we tried to find a correlation between the spontaneous in vitro immunoglobulin synthesis from patients' peripheral blood lymphocytes and the pattern of S6F1 expression. Although the total number of double-positive CD8+/S6F1+ cells was similar in both HIV-1+ and HIV-1- haemophiliac patients, a significant increase in the CD8+/S6F1+ population bright versus dim was documented in HIV-1-infected with respect to HIV-1 haemophiliacs (bright/dim ratio 3·97 ± 0·61 versus 0·75 ± 0·1, respectively, P &lt; 0·005). This finding was correlated to a significant increase in spontaneous in vitro immunoglobulin production in HIV-1+ subjects compared with control haemophiliacs (P &lt; 0·005). Purified CD8+ lymphocytes from HIV-1+ subjects showed a reduced suppressor activity on mitogen-induced immunoglobulin production. Taken together, these data suggest that HIV-1 infection favours the generation of CD8+/S6F1+ bright cells with putative cytotoxic-associated function, leading to a progressive reduction in the number of CD8+/S6F1+ dim suppressor lymphocytes. This phenomenon may contribute to the polyclonal hypergammaglobulinaemia present in HIV-1+ haemophiliac patients.
The induction of cell-associated and secreted IL-1 by iscoms, matrix or micelles in murine splenic cells
Authors: VILLACRES-ERIKSSON M , BERGSTRÖM-MOLLAOGLU M , KÅBERG H , LÖVGREN K , MOREIN B 
Published: July 2010

SUMMARYThe kinetics of the expression of membrane-associated IL-1 (mIL-1) and soluble IL-1 (sIL-1) was studied in in vitro stimulated spleen cells from non-primed mice or from mice primed with influenza virus antigens incorporated in the immuno-stimulating complexes (iscoms) or as micelles. Matrix, which is the carrier structure for the antigens in the iscom, was used as a non-antigen stimulus. The IL-1 produced was assayed in an IL-1-dependent cell line and the specificity was demonstrated in a blocking experiment with antiserum to IL-1α. Soluble IL-1α was also quantified in ELISA. Iscoms and matrix induced production of mIL-1 and sIL-1 in cultures from non-treated mice as well as from mice primed 4 days before with iscoms or micelles. Micelles were a less strong stimulus and did not induce production of sIL-1. Micelles induced production of mIL-1 in cultures from non-primed mice or from mice which were recently immunized with micelles. No mIL-1 expression was induced by micelles if the spleen cells originated from mice immunized shortly before with iscoms. Depletion experiments demonstrated that sIL-1 was produced by adherent cells upon stimulation with iscoms or matrix. However, factor(s) from the non-adherent cells seem to be necessary for optimal secretion of sIL-1.
Long-term ultraviolet B-induced impairment of Langerhans cell function: an immunoelectron microscopic study
Authors: VAN PRAAG M C G , MULDER A A , CLAAS F H J , VERMEER B-J , MOMMAAS A M 
Published: July 2010

SUMMARYThe influence of low-dose, long-term ultraviolet B (UVB) light exposure on HLA class Il-positive human epidermal Langerhans cells (LC) was studied using a sensitive immunoelectron microscopic technique for the ultrastructural assessment of HLA class II expression on LC and for quantification of these cells in situ. Six healthy Caucasian volunteers participated in the experiments and received thrice weekly UVB treatments for 4 weeks. The initial dose ranged from 30 to 50mJ'cnv and the total dose from 600 to 3500 mJ/cm2, depending on skin type. Suction blisters and biopsies were obtained before the start of the UVB protocol and 48 h after the last UVB irradiation, and processed for the mixed epidermal cell-lymphocyte reaction (MECLR) and electromicroscopy, respectively, The MECLR was used as a measure of the immune response. The distribution of HLA class 11 molecules on LC was studied by incubating ultrathin cryosections of human skin tissue with an anti-HLA class II MoAb that was conjugated to 10 nm colloidal gold. Furthermore the number of LC was assessed ultrastructurally, when they could be recognized by their unique cytoplasmic organdie, the Birbeck granule (BG). The UVB protocol that was employed caused a marked suppression of the MECLR responses. This UVB-induced reduction of the immune response was not paralleled by changes in HLA class II expression on LC. nor in the number of epidermal LC. These findings are further support for our hypothesis that UVB-induced immune suppression in the skin is not due to a depletion of local LC.
Anti-αβ T cell receptor antibody prevents the progression of experimental autoimmune myocarditis
Authors: HANAWA H , KODAMA M , INOMATA T , IZUMI T , SHIBATA A , TUCHIDA M , MATSUMOTO Y , ABO T 
Published: July 2010

SUMMARYWe investigated the effects of anti-αβ T cell receptor antibody in rat experimental autoimmune myocarditis (HAM), using a new animal model of autoimmune myocarditis characterized by the appearance of multinucleated giant cells. KAM was induced by injecting Lewis rats subcutaneously in the footpads with 1.0 mg of human cardiac myosin in an equal volume of Freund's complete adjuvant (FCA) on days 0 and 7. In experiment 1, we evaluated the effect of long-term anti-αβ TCR antibody therapy on prevention of progression of EAM. Long-term administration of anti-αβ TCR antibody prevented progression of FAM in a dose-dependent manner. Flow cytometry performed at the time of sacrifice showed that the percentage of αβ T cells in lymph nodes and spleen was similar in the control group and the group in which almost no histologic evidence of myocarditis was found. In experiment 2, we examined the effects of short-term therapy. Rats were killed at different stages and pathologic specimens were examined. Short-term therapy delayed the onset of myocarditis. Results of flow cytometry suggested that impairment of antigen recognition or T cell function by occupancy of the TCR rather than depletion of TCR was the mechanism responsible for suppression of EAM.
Development of antibodies to hepatitis B virus surface antigen in bone marrow transplant recipient following treatment with peripheral blood lymphocytes from immunized donors
Authors: ILAN Y , NAGLER A , SHOUVAL D , ACKERSTEIN A , OR R , KAPELUSHNIK J , ADLER R , SLAVIN S 
Published: July 2010

SUMMARYBone marrow transplantation (BMT) recipients are immunosuppressed and are at risk for contracting severe infections. Recently, adoptive transfer of immunity against hepatitis B virus (HBV) was documented in BMT recipients receiving bone marrow from ‘naturally’ HBV-infected individuals who recovered spontaneously, or those transplanted with bone marrow cells obtained from actively immunized donors. Furthermore, reconstitution of the immune system in a BMT recipient who was a hepatitis surface antigen (HBsAg)+/HBV DNA+ carrier with HBV immune bone marrow ceils led to clearance of the replicating virus, presumably through adoptive cell-mediated immunotherapy. We report three cases of induction of immunity to HBV by selective adoptive transfer by i.v. injection of peripheral blood lymphocytes (PBL) obtained from BMT donors who were actively immunized against HBV after harvesting of bone marrow. Ail three BMT recipients developed anti-HBs antibodies. In one BMT case in whom antibodies to HBsAg developed following adoptive transfer of immune PBL, a mild booster effect was documented in the BMT recipient upon immunization with a recombinant hepatitis B vaccine. The two remaining patients lost their antibodies to HBsAg in association with relapse of leukaemia. This immune manipulation may open the door to evaluation of adoptive transfer of immunity to HBV through selective transplantation of HBV immune lymphocytes in selected patients such as those with persistent HBV infection, as well as liver transplant recipients who require protection of the graft against HBV re-infection.
Binding of mannan-binding protein to various bacterial pathogens of meningitis
Authors: VAN EMMERIK L C , KUIJPER E J , FIJEN C A P , DANKERT J , THIEL S 
Published: July 2010

SUMMARYMannan-binding protein (MBP), a calcium-dependent plasma lectin, may play a role in the innate defence against microorganisms. After binding lo carbohydrate structures at the bacterial surface, MBP activates the classical pathway of the complement system. To investigate the binding capacity of MBP to various bacteria associated with meningitis, an assay was developed to study the binding of MBP to bacteria grown in a semisynthetic fluid culture medium. Salmonella montevideo (containing a mannose-rich lipopolysaccharide (LPS)), used as a positive control strain, showed binding of radiolabelled MBP at a level of 80% compared with binding of MBP to zymosan. Binding of labelled MBP to Salm. montevideo was time-dependent, temperature-dependent and saturable. The binding, was inhibited by unlabelled MBP., by mannose and by N-acetyl-o-glucosamine. Among bacterial pathogens often found to cause meningitis, a wide range of MBP binding capacities could be determined. The encapsulated Neisseria meningitidis (representatives from 11 serogroups other than group A were included: n = 22), N. mucosa (n = 1), Haemophilus influenzae type b (n = 10) and Streptococcus agalactiae (n = 5) had a low MBP binding capacity of 21.7% (95% confidence interval (Cl) 3.3–40.1%). Escherichia coli K1 (n = 11). Strep, suis (n = 5), Strep, pneumoniae (n = 10) and N. meningitidis scrogroup A (n = 2) showed intermediate MBP binding capacity of 58.4% (95% Cl 40.0–76.8%). A third group consisting of non-encapsulated Listeria monocytogenes (n = 11), non-encapsulated H. influenzae (n = 2), non-encapsulated N. meningitidis (n = 2), N. cinera (n = 1) and N. subflava (n = 1) strains had a high MBP binding capacity of 87.5% (95% CI 62.5–12.5%). The majority of encapsulated pathogens causing bacterial meningitis seem to have a rather low MBP binding capacity.
Increased levels of interferon-gamma (IFN-γ), IL-4 and transforming growth factor-beta (TGF-β) mRNA expressing blood mononuclear cells in human HIV infection
Authors: NAVIKAS V , LINK J , WAHREN B , PERSSON Ch , LINK H 
Published: July 2010

SUMMARY
Evidence has been presented for the involvement of IFN-γ, IL-4 and TGF-β in AIDS. Measured plasma levels may, however, poorly reflect in vivo production, since cytokines act auto- and paracrinally and have very short half life in plasma. In situ hybridization with complementary DNA oligonucleotide probes was used lo enumerate blood mononuclear cells expressing cytokine messenger RNA(mRNA). HIV-infected patients had elevated blood levels of cells expressing each of the cytokines, with predominance for cells expressing TGF-β mRNA. All AIDS patients included had elevated numbers of IL-4 mRNA-expressing cells, and levels of cells expressing this cytokine correlated inversely with counts of CD4+ cells in blood, reflecting the involvement of Th2-like cells in later stages of HIV infection. The described approach should be useful in further studies of cytokines in HIV infection and other diseases.
Generation and characterization of a continuous line of CD8+ suppressively regulatory T lymphocytes which down-regulates experimental autoimmune orchitis (EAO) in mice
Authors: MUKASA A , HIRAMINE C , HOJO K 
Published: July 2010

SUMMARYWe have previously shown that two injections with viable syngeneic testicular germ cells (TC) alone developed experimental autoimmune orchitis (EAO) in C3H/He mice, and that the induction of antigen-specific tolerance in this EAO model is associated with the generation of antigen-specific suppressively regulatory T (Ts) cells. For the elucidation of the nature of these Ts cells, a murine Ts cell line (designated Ts-A) was established. This line was generated from the spleen cells of C3H/He mice which had received three i.v. injections of a soluble (deaggregated) form of murine testicular antigen (mTA), followed by the repeated selection of these spleen lymphocytes in vitro by stimulation with mTA. Adoptive transfer of Ts-A cells into naive syngeneic mice immediately before the first TC injection was found to downgrade EAO in actively immunized recipients. The transferred Ts-A cells significantly inhibited the cellular immune response to TC in the recipients in an antigen-specific manner, but these cells had no inhibitory effect on the humoral immune response to TC. This line could also inhibit in vitro syngeneic TC-driven proliferation of orchitogenic lymphocytes. Surface phenotype of this line was GD8+, GD4−, Thy-1.2+, CD3 +, and TGR αβ+. These findings may suggest an in vivo role for suppressively regulatory lymphocytes, capable of inhibiting helper T cells, in the regulation of EAO.
The costimulatory signal CD28 is fully functional but cannot correct the impaired antigen response in T cells of patients with common variable immunodeficiency
Authors: FISCHER M B , WOLF H M , EGGENBAUER H , THON V , VOGEL E , LOKAJ J , LITZMAN J , MANNHALTER J W , EIBL M M 
Published: July 2010

SUMMARYA wide spectrum of different immunologic abnormalities have been postulated as being responsible for the impairment of specific antibody production and the decrease in all or selected immunoglobulin isotypes present in common variable immunodeficiency (CVID). These abnormalities include impaired B cell differentiation and or function, defective macrophage function, and significant T cell detects. The aim of the present study was to delineate whether the accessory molecule CD28 is involved in the impaired antigen response of T cell from patients with CVID. Our results demonstrate that CD28 costimulation was functional in T cells stimulated with anti-CD3 or anti-TCR MoAb. but could not correct the impaired response of patients' peripheral blood T cells to tetanus toxoid. Analysis of patients' long-term cultured T cells further confirmed these results. Exogenous rIL-2, another costimulus, augmented but did not correct the defective proliferation and lymphokine production in patients' antigen-driven peripheral blood T lymphocytes or in long-term cultured T cells. These findings indicate that the CD28 signalling pathway in these patients'T cells is unimpaired, and that costimulation via CD28 cannot correct the defect occurring in the course of TCR-mediated T cell activation.
Antigen presentation by macrophages from bacille Calmette-Guérin (BCG)-resistant and -susceptible mice
Authors: HILBURGER M E , ZWILLING B S 
Published: July 2010

SUMMARYWe have compared the antigen-presenting capacity of macrophages from congenic BALB/c.Bcgr and BALB/c.Bcgs mice that differentially express MHC class II glycoproteins. Several different criteria were used to evaluate the presentation of a protein antigen, ovalbumin (OVA), including limiting the concentration of antigen or the numbers of macrophages, and using both native OVA and OVA peptide 323–339. No differences in the capacity of macrophages from Bcgr and Bcgs mice to present antigen to a OVA-specific T cell hybridoma were found. Splenic macrophages from BCG-infected congenic mice also induced an equivalent amount of IL-2 production by the T cell hybridoma. The relationship of these findings to other differences that have been attributed to Bcg are discussed.
Complement inhibition by human vitronectin involves non-heparin binding domains
Authors: SHEEHAN M , MORRIS C A , PUSSELL B A , CHARLESWORTH J A 
Published: July 2010

SUMMARYVitronectin (complement S-protein), a multifunctional glycoprotein, inhibits complement-mediated cytolysis at two identified stages of terminal complement complex (TCC) formation: blocking of C5b-7 membrane binding, and prevention of C9 polymerization. However, the functional domain(s) of vitronectin involved in these reactions remains incompletely defined. In order to identify the complement inhibition site, a 12-kD heparin binding fragment and two other internal fragments (53kD and 43 kD) of vitronectin were isolated after cyanogen bromide (CNBr) treatment of the native molecule. Potent inhibition of guinea pig erythrocyte (GPE) reactive lysis was demonstrated with native vitronectin, total CNBr digest and the 53-kD and 43-kD fragments, but only very poorly by the heparin binding 12-kD peptide. Similarly, the 43-kD fragment blocked the binding of C5b-7 to immobilized vitronectin, whereas the 12-kD fragment had no effect. These data localize the C5b-7 binding site to a 43-kD internal region. Further characterization of the fragments was carried out in an assay which detected C9 polymerization in the presence of C5b-8. Polymerized material was separated by PAGE, detected by autoradiography and quantified after excision from the gels. Results showed that polymerization did not occur in the presence of the 53-kD and 43-kD fragments. However, the 12-kD heparin binding fragment had no effect. It is proposed that prevention of C5b-8-induced C9 polymerization resides at a site in an internal region of the vitronectin molecule.
Participation of CR1 (CD35), CR3 (CD11b/CD18) and CR4 (CD11c/CD18) in membranoproliferative glomerulonephritis type I
Authors: SOMA J , SAITO T , SEINO J , SATO H , OOTAKA T , YUSA A , ABE K 
Published: July 2010

SUMMARYIntraglomerular expression of complement receptors (CR) was investigated chronologically in 22 repeatedly biopsied patients with membranoproliferative glomerulonephritis (MPGN) type I by indirect immunoperoxidase staining using MoAbs. Patients were divided into two groups based on whether intraglomerular C3c deposition was decreased at the second biopsy (2nd Bx) (group A, n= 12), or not (group B, n= 10). At the first biopsy (1st Bx), the severity of glomerular injury and the degree of glomerular C3c deposition were compatible between the two groups. Four patterns of CR1 (CD35) expression on podocytes were recognized: normal; generally decreased; focally/ segmentally lost; and completely lost. The numbers of CR3 (CD11b/CD18)- and CR4 (CD11c/ CD18)-positive cells per glomerular cross-section were counted. At the 1st Bx, no significant difference was found in the number of CR3+ or CR4+ cells between the two groups. At the 2nd Bx. the numbers of both the CR3+ and CR4+ cells were significantly decreased only in group A (P &lt;0·01). The numbers of CR3+ and CR4+ cells were significantly higher in cases with moderate or marked C3c deposits than in those with no or mild C3c deposits. The intensity of CR1 expression in group B was less than that in group A at both the 1st and 2nd Bx (1 st, P &lt;0·05; 2nd, P &lt; 0·01), and chronological improvement of CR1 expression was observed only in group A. The severity of glomerular injury was increased only in group B (P &lt;0·01), and was associated with persistent massive proteinuria and hypocomplementaemia. Our results suggest that, in cases with an adverse outcome, a more severe defect of CR1 initially exists and the expression of CR1 is not recoverable chronologically. This irreversible decrease or loss of CR1 may partly contribute to the continuous C3c deposition and intraglomerular infiltration of CR3+ and CR4+ cells.
Occurrence of disseminated Intravascular coagulation (DIC) in active systemic anaphylaxis: role of platelet-activating factor
Authors: CHOI I H , HA T Y , LEE D G , PARK J S , LEE J H , PARK Y M , LEE H K 
Published: July 2010

SUMMARYThe possible occurrence of DIC in active systemic anaphylaxis was investigated in mice. Induction of active systemic anaphylaxis resulted in the development of DIC symptoms such as thrombo-cytopenia, prolongation of prothrombin time, hypofibrinogaemia, and elevated level of fibrinogen/fibrin degradation products. In addition, in histological examinations, massive congestion and cellular infiltration in pulmonary interstitia, and considerable haemorrhage in renal medullae were observed. All these changes were nearly completely prevented by pretreatment with platelet-activating factor (PAF) antagonist (BN 50739). Moreover, the same haematological and morphological changes were produced by a bolus injection of PAF. These data strongly suggest that DIC occurs in active systemic anaphylaxis and PAF plays a pivotal role in the development of DIC in anaphylaxis.
Expression of the B cell repertoire inlprmice; abnormal expansion of a few VHJ558 germ-line genes
Authors: AlarcÓN-Riquelme M E , FernÁNdez C 
Published: July 2010

SUMMARYAnalysis of the VH gene repertoire of the J558 family was done in lipopolysaccharide (LPS)-stimulated resting cells and in vivo activated cells derived from C51B1/6-lpr mice (IghCb). Using a restriction fragment length polymorphism (RFLP) based on digestion with the restriction enzyme Pst l, the expression of the subfamilies of the J558 family of VH genes could be determined. The J558 subfamily repertoire of resting B cells of the lpr mice was similar to that of the normal mice, while the J558 repertoire of the in vivo-activated cells was altered: analysis and sequencing of the IgM-expressed J558 repertoire of a sick female mouse showed that 50% of the J558 genes were represented by a single VH gene rearrangement, showing that its expansion was monoclonal. Furthermore, this same rearrangement made up to 90% of the J558 repertoire in the IgG2a+ population, showing that it had been preferentially selected, expanded and switched. However, compared with its IgM counterpart, it showed no evidence of somatic hypermutation.
The pyrimidin analogue cyclopentenyl cytosine induces alloantigen-specific non-responsiveness of human T lymphocytes
Authors: Nikolaeva N , Bemelman F J , Yong S-L , Verschuur A , van Lier R A W , ten Berge I J M 
Published: July 2010

Summary
Cyclopentenyl cytosine (CPEC) has been shown to induce apoptosis in human T lymphoblastic cell lines and T cells from leukaemia patients. In this study we have addressed the question of whether CPEC is able to decrease proliferation and effector functions of human alloresponsive T lymphocytes and induce T cell anergy. The proliferative capacity of human peripheral blood mononuclear cells in response to allogeneic stimulation was measured by 5,6-carboxy-succinimidyl-diacetate-fluorescein-ester staining. Flow cytometric analysis was performed using surface CD4, CD8, CD25, CD103 and intracellular perforin, granzyme A, granzyme B, caspase-3 and forkhead box P3 (FoxP3) markers. The in vivo immunosuppressive capacity was tested in a murine skin graft model. Addition of CPEC at a concentration of 20 nM strongly decreased the expansion and cytotoxicity of alloreactive T cells. Specific restimulation in the absence of CPEC showed that the cells became anergic. The drug induced caspase-dependent apoptosis of alloreactive T lymphocytes. Finally, CPEC increased the percentage of CD25high FoxP3+ CD4+ and CD103+ CD8+ T cells, and potentiated the effect of rapamycin in increasing the numbers of alloreactive regulatory T cells. Treatment with CPEC of CBA/CA mice transplanted with B10/Br skin grafts significantly prolonged graft survival. We conclude that CPEC inhibits proliferation and cytotoxicity of human alloreactive T cells and induces alloantigen non-responsiveness in vitro.