bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increased expression of IgG Fc receptor type I on neutrophils and monocytes from HIV-infected subjects
Authors: CAPSONI F , MINONZIO F , ONGARI A M , COLOMBO G , RIZZARDI G P , BONARA P , D'ARMINIO-MONFORTE A , ZANUSSI C 
Published: August 2010

SUMMARYInterferon-gamma (IFN-γ) induces de novo expression of IgG Fc receptor type I (FcRI) on neutrophils and significantly raises the level of these receptors on monocytes. Since increased concentrations of IFN-γ have been observed in sera from patients with HIV infection, FcRI expression might also be increased on these subjects' phagocytes. FcRI expression was assessed by indirect immunofluorescence staining of phagocytes in whole blood from 40 healthy controls and 55 HIV+ subjects, 24 belonging to CDC class III and 31 to CDC class IV; 42 were intravenous drug abusers (IVDA) and 13 were homosexual men. Plasma levels of IFN-γ were measured using a modified immunoradiometric assay. The mean linear fluorescence intensity, used as a relative measure of receptor expression, was significantly higher on unseparated neutrophils from HIV+ subjects in CDC classes III (P&lt;0·001) and IV (P &lt; 0·0001) than from controls. Similar changes in FcRI expression were observed on monocytes from HIV+ subjects. While no differences were observed between IVDA and homosexual HIV+ patients, there was a significant association between FcRI expression and the patients' CDC stage, those in class IV having the highest FcRI levels. Plasma IFN-γ concentrations were significantly higher in HIV + patients than in controls and a positive correlation with the stages of HIV infection was again observed. FcRI expression was also increased on freshly purified neutrophils from five HIV+ patients in CDC class IV but did not increase further after 18 h incubation with IFN-γ, a treatment that up-regulated FcRI expression on control neutrophils. These data suggest that: (i) FcRI evaluation may be a sensitive marker for the biological activity of IFN-γin vivo; (ii) phagocytes from HIV+ subjects are activated in vivo by IFN-γ, expressing increased levels of FcRI; (iii) these IFN-γ-activated cells may play a role in the pathogenesis of AIDS.
Natural killer (NK) cell activity during HIV infection: a decrease in NK activity is observed at the clonal level and is not restored afterin vitrolong-term culture of NK cells
Authors: SCOTT-ALGARA D , VUILLIER F , CAYOTA A , DIGHIERO G 
Published: August 2010

SUMMARYNK cell activity is impaired in HIV-infected patients. The mechanisms behind the altered NK functions are not clear, and conflicting data concerning NK and antibody-dependent cellular cytotoxicity (ADCC) activity have been reported. In order to investigate whether this impairment is also observed at the clonal level and whether it is related to a defect at the target cell binding and/or the post-binding level, we evaluated highly purified NK cell lines and cloned NK cells obtained from 22 HIV-infected patients at different stages of disease and compared them with normal controls for their ability to: (i) kill K-562 and U-937 cell lines using a 51Cr release assay; (ii) bind and kill K-562 and U-937 cells at the single cell binding level; (iii) release NK cytotoxic factor (NKCF), tumour necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ); (iv) kill anti-IgM preincubated Daudi cell line (ADCC activity). This study with cloned NK cells or NK cell lines from HIV-infected individuals showed: (i) a decrease in their lytic capability against target cell lines; (ii) a low ability to form conjugates with K-562 and U-937 cell lines with respect to controls; (iii) a decreased ability to kill bound target cells; (iv) low levels of released NKCF, TNF-α and IFN-γ after incubation with U-937 cells. Taken together, these findings suggest that the impaired NK cell function during HIV infection is also observed at the clonal level and is related to defects both at the target and post-binding levels. However, the precise mechanisms remain to be determined. The inability to restore normal NK activity after long-term culture in the presence of high levels of recombinant IL-2 is in agreement with the hypothesis of a ‘general anergic process’ during HIV infection.
Cellular immunity in tuberculous pleural effusions: evidence of spontaneous lymphocyte proliferation and antigen-specific accelerated responses to purified protein derivative (PPD)
Authors: LORGAT F , KERAAN M M , RESS S R 
Published: August 2010

SUMMARYThe kinetics of in vitro cellular proliferation against a PPD of Mycobacterium tuberculosis or streptococcal antigen (streptokinase-streptodornase) was evaluated in pleural fluid and peripheral blood mononuclear cells (PBMC) from patients with tuberculous and non-tuberculous pleuritis. The peak proliferative response to PPD by mononuclear cells from pleural fluid occurred earlier (day 3) in 65% of patients with tuberculosis, a finding not seen in non-tuberculous effusions. Spontaneous lymphocyte proliferation of both peripheral blood lymphocytes and pleural effusion lymphocytes was frequently observed, irrespective of etiology. However, 20 of 21 tuberculous patients manifesting spontaneous lymphocyte proliferation had accelerated kinetics of proliferation to PPD, which was antigen-specific. These results suggest that spontaneous lymphocyte proliferation occurs as a response to antigen stimulation at the site of disease, and is not a non-specific response to inflammation. Furthermore, enhanced reactivity against mycobacterial antigen, manifested by accelerated kinetics of proliferation, has diagnostic potential in patients with pleural effusions.
Detection and characterization of immunoconglutinins in patients with systemic lupus erythematosus (SLE): serial analysis in relation to disease course
Authors: NILSSON B , NILSSON EKDAHL K , SJÖHOLM A , NILSSON U R , STURFELT G 
Published: August 2010

SUMMARYThe levels of IgA, IgG and IgM immunoconglutinins (IK) were assessed in sera from 20 patients with SLE which were followed for 8-month periods. At the time of the exacerbation, IgG IKs were significantly increased to 226 ± 90 arbitrary units (mean ± s.e.m.) compared with both the minimum value of 75 ± 28 in the SLE patients and with 31 ± 2 in healthy controls (P &lt;0·05). There was no difference between SLE patients and controls in the levels of IgM and IgA IKs. Most of the SLE patients in this material showed maximal IgG IK levels before exacerbation, but there was no correlation between the clinical disease index and the levels of IgG IK. The specificity of IgG IKs showed a broad diversity for microtitre-fixed C3b, iC3b, C3c and C3dg. The antibodies were of IgG1, IgG3 and in two patients, IgG4 subclass. IgG IKs were correlated to the C3d/C3 ratio which suggested that the IK responses were secondary to C3 activation. In summary, unlike other conditions associated with complement activation where elevated IgM IKs are common, an increase in IgG IK levels was observed. It is possible that this diverging IK response contributes to the pathophysiology of the disease.
The putative role of cytokines in the induction of primary anti-phospholipid syndrome in mice
Authors: FISHMAN P , BAKIMER R , BLANK M , SREDNI D , DJALDETTI M , SHOENFELD Y 
Published: August 2010

SUMMARYAntiphospholipid syndrome (APLS) is characterized by thrombocytopenia, thromboembolic phenomena and recurrent fetal loss, associated with anti-cardiolipin antibodies (ACA) and/or lupus anticoagulant. The syndrome may be primary or may be associated with other conditions such as systemic lupus erythematosus (SLE). In this study we induced primary APLS following immunization of BALB/c mice with a human monoclonal ACA (H-3). Analysis of the cytokine profile of the mice with experimental APLS indicated low production of IL-2, IL-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF) by concanavalin A (Con A)-slimulated splenocytes of H-3 immunized mice. It seems that the low levels of IL-3 and GM-CSF have a potential role in the fetal loss of the APLS. Whatever the mechanism of IL-3 and GM-CSF in preventing fetal loss, these results may have therapeutic bearing on the reproductive outcome in women and other species with APLS.
Expression of T cell receptors αβ and γδ in the ileal mucosa of patients with Crohn's disease and with spondylarthropathy
Authors: CUVELIER C A , DE WEVER N , MIELANTS H , DE VOS M , VEYS E M , ROELS H 
Published: August 2010

SUMMARYThe expression of the αβ and γδ heterodimer of the T cell receptor (TCR) was studied in normal human ileal mucosa or in ileal biopsies featuring Crohn's disease or acute and chronic spondylarthopathy-related gut inflammation. With an immunohistochemical technique we demonstrated that the increase of mucosal lymphocytes per mm mucosa in Crohn's disease and spondylarthropathy-related ileitis is exclusively due to expansion of the αβ+ T cell compartment. In Crohn's disease and chronic ileitis observed in some spondylarthropathy patients the αβ+ T cells were increased amongst intraepithelial lymphocytes (IEL). The lamina propria lymphocytes (LPL) were augmented in all studied inflammatory conditions. The γδ+ T cells showed no changes in IEL or LPL and their proportions were not altered. They were evenly dispersed throughout the ileal mucosa and did not seem to participate in the inflammatory process. This study confirms that γδ T cells are a distinct subset in the intestinal mucosa. The increase in αβ+ T cells suggests augmented mucosal antigen handling and involvement of the major histocompatibility complex in the pathogenesis of spondylarthropathy-related gut inflammation and Crohn's disease.
The role of T cells and the effect of hydrocortisone on interleukin-4-induced IgE synthesis by non-T cells
Authors: NÜSSLEIN H G , TRÄG T , WINTER M , DIETZ A , KALDEN J R 
Published: August 2010

SUMMARYThe role of T cells for IL-4-induced IgE synthesis by peripheral blood mononuclear cells (PBMC) was investigated. The removal of monocytes from PBMC abolished IL-4-induced IgE synthesis. When PBMC were separated into T and non-T cells, non-T cells alone were not able to secrete significant amounts of IgE in the presence of IL-4. Depending on the separation procedure, the reconstitution of non-T cells with T cells prepared by rosetting did not restore IgE secretion, whereas T cells obtained by the use of anti-CD3 antibodies could co-induce IgE formation. However, when the T cells were first irradiated, large amounts of IgE were produced, which strongly exceeded those found in unscparated PBMC cultures. IL-4-induced IgE synthesis was also obtained in co-cultures of formaldehyde-fixed T cells with non-T cells. Furthermore, not only autologous but also allogeneic T cells, which have been irradiated or fixed, could provide the costimulatory effect on IgE formation by non-T cells in the presence of IL-4. Mitogenically pre-activated T cells, however, were not able to support IgE synthesis. Hydrocortisone (HC) potentiated the IL-4-induced IgE synthesis by PBMC and enabled non-T cells to secrete IgE in the presence of IL-4. Adding both HC and T cells led to a marked synergistic effect on IL-4-induced IgE production. We conclude that monocytes are required for the induction of IgE synthesis in PBMC in addition to T cells and IL-4. Our results support the view that the T cell signal is delivered via cognate and non-cognate T/B cell membrane interaction. Furthermore, active and proliferating T cells rather suppress IgE synthesis. Finally, HC appears to be a potent alternative stimulus, which bypasses the necessity for T cells in IL-4-induced IgE formation.
Production of serum amyloid A and C-reactive protein by HepG2 cells stimulated with combinations of cytokines or monocyte conditioned media: the effects of prednisolone
Authors: SMITH J W , McDONALD T L 
Published: August 2010

SUMMARYThe hepatic production of the acute phase proteins in response to inflammatory cytokines, and the interaction of corticosteroids within this response, has been the subject of considerable recent research. In this study we have examined the effects of the corticosteroid prednisolone on the production of IL-1α and IL-I/β by lipopolysaccharide(LPS)-stimulaied monocytes, and the ability of the monocyte conditioned media (MOCM) obtained under these conditions to induce human hepatoma HepG2 cells to produce serum amyloid A (SAA) and C-reactive protein (CRP). We also examined the production of SAA and CRP by HepG2 cells exposed to different combinations and concentrations of recombinant human (rh) IL-lα, rhIL-1/β rhIL-6, recombinant human tumour necrosis factor-alpha (rhTNF-α) and prednisolone. The findings indicate: (i) prednisolone substantially inhibits the production of both IL-lα and IL-lβ by LPS-stimulated monocyles. The MOCM from prednisolone-treated monocyles induced less SAA and CRP production by HepG2 cells; (ii) IL-1α and IL-1β both induced CRP and SAA synthesis by HepG2 cells, but only in the presence of IL-6. IL-lβ was the more potent inducer for SAA production, but for CRP production IL-1α and IL-lβ were equivalent; (iii) prednisolone enhances the production of SAA by HepG2 cells, but docs not enhance the production of CRP; (iv) TNF-a in the presence or absence of IL-6 and/or prednisolone did not induce the production of SAA or CRP by HepG2 cells. These findings offer a tenable solution to a disparate production of SAA compared with CRP in corticosteroid-treated cystic fibrosis (CF) patients.
The acquisition of anti-pneumococcal capsular polysaccharideHaemophilus influenzaetype b and tetanus toxoid antibodies, with age, in the UK
Authors: HAZLEWOOD M , NUSRAT R , KUMARARATNE D S , GOODALL M , RAYKUNDALIA C , Da WANG GONG , JOYCE H J , MILFORD-WARD A , FORTE M , PAHOR A 
Published: August 2010

SUMMARYAntibody levels specific for capsular polysaccharides of Streptococcus pneumoniae and Haemophilus influenzae type b (Hib) and to tetanus toxoid (TT). were measured in serum samples of 750 age-stratified subjects from the UK. The study subjects comprised healthy adult volunteers and hospitalized children undergoing elective surgery, excluding those with a history of infection or under investigation for immunological or haematological disorders. These antibody levels were calibrated by comparison with serum pool obtained from healthy adult volunteers, who were immunized with Hib polyribose-phosphate vaccine (Merieux). The data are intended to provide reference ranges to assist in the interpretation of specific antibody measurements in the clinical setting. Maternal IgG pneumococcal capsular polysaccharide (PCP) specific antibody levels, geometric-mean titre (GMT) 1/22, were lost by 6 months of age (GMT of 1/9). They remained low until 3–5 years (GMT of 1/20), and consisted principally of IgGl. Thereafter, IgG anti-PCP antibody titres increased steadily to adult levels (GMT of 1/275), of which 80% was IgG2. Anti-PCP antibody titres of the IgM isotype rose steadily from a GMT 1/21 (0–6 months) to 1/420(3–5 years), a level which was maintained until adulthood. Anti-Hib antibody concentrations, determined by RABA, again demonstrated the decline in maternal antibody, from 0.18 μg/ml in the 0.6 month age cohort, to 0.09 μg/ml between 6 and 12 months. Geomctric-mcan antibody concentrations remained below 0.2 μg/ml until 3–5 years, then increased with age, attaining the mean adult level of 1.02 μg/ml. Anti-TT antibody concentrations were measured in the same sera, by ELISA. Two peaks in anti-TT antibody levels were seen in children of 0.059 IU/ml and 0.166 IU/ml corresponding to the schedule of routine childhood immunization in the first year and at 5 years of age.
A comparison of the T cell delayed-type hypersensitivity epitopes of the 19-kD antigens fromMycobacterium tuberculosisandMyco. intracellulareusing overlapping synthetic peptides
Authors: MACKALL J C , BAI G H , ROUSE D A , ARMOA G R G , CHUIDIAN F , NAIR J , MORRIS S L 
Published: August 2010

SUMMARYMycobacterial disease remains a serious international public health concern. Improved methods to rapidly and specifically detect mycobacterial infections would greatly enhance clinical management of these diseases. To define species-specific T cell epitopes that may be useful for the immunodiagnosis of mycobacterial infections, polymerized synthetic peptides from the 19-kD Mycobacterium tuberculosis and Myco. intracellulare protein homologues were tested in guinea pig DTH assays. Five Myco. tuberculosis and eight Myco. intracellulare peptides evoked skin test responses. Although all of the active Myco. tuberculosis and seven of the Myco. intracellulare peptides elicited non-specific DTH reactions, the peptide IN13 induced a Myco intracellulare-specific skin test reaction, and thus represents a specific Myco intracellulare T cell DTH epitope. This result suggests that the development of monospecific peptide-based immunodiagnostic reagents may be feasible for future clinical use.
Production of IL-1 and IL-1 receptor antagonist and the pathological significance in lipopolysaccharide-induced arthritis in rabbits
Authors: MATSUKAWA A , OHKAWARA S , MAEDA T , TAKAGI K , YOSHINAGA M 
Published: August 2010

SUMMARYInjection of lipopolysaccharide (LPS) into rabbil knee joints provoked leucocyte infiltration and loss of proteoglycan (PG) from the cartilage. We investigated the role of IL-1 and IL-1 receptor antagonist (IL-IRa) and its significance in the pathogenesis of LPS-arthritis. Production of IL-1β peaked at 6 h (196.7±89.4 pg/joint) after injection of 10 ng of LPS. while IL-IRa peaked at 9 h (34.5 ± 13.4 ng/joint). The amount of IL-IRa was 180–200-fold molar excess of IL-1, and a large amount of IL-IRa was sustained for I week. Both IL-1β and IL-IRa were mainly produced by synovial exudate cells. Arthritis was reproduced by rabbit IL-1β. LPS-induced leucocyte infiltration was inhibited 70–75% by rabbit IL-IRa. Loss of PG in LPS-arthritis was prevented by IL-1Ra and also by neutrophil elastase inhibitor, and superoxide dismutase. In leucopenic rabbits, injection of LPS induced neither production of IL-1β nor loss of PG. Direct injection of inflammatory exudated cells in leucopenic rabbits reproduced loss of PG. and there was only a partial recovery by IL-1Ra. These results suggest that LPS-initiated IL-1 acts as a key mediator in LPS-arthritis and that endogenous IL-1 Ra may suppress a part of IL-1 activity at the site, but its amount was too low for suppression of the produced IL-1. Loss of PG is a sequela of infiltrated leucocytes and leucocyte-derived elastase, and superoxide anion may play a pivotal role in the destruction of cartilage.
IL-2 enhances polyclonal IgM but not IgM-rheumatoid factor synthesis by activated human peripheral blood B cells
Authors: CALLAGHAN M , WHELAN A , FEIGHERY C , BRESNIHAN B 
Published: August 2010

SUMMARYIgM-rheumatoid factor (RF) is thought to be involved in the pathogenesis of rheumatoid arthritis (RA). Several cytokines are known to regulate immunoglobulin synthesis. In this study the effects of IL-2 on polyclonal IgM and IgM RF synthesis were compared. Cytokines were added to peripheral blood B cells from normal subjects and patients with RA after activation by Staphylococcus aureus Cowan 1 (SAC). The addition of IL-2. but not IL-4 or IL-6, resulted in significant enhancement of IgM synthesis in cultures from both healthy subjects and patients with RA. Similar degrees of enhancement were seen in both peripheral blood mononuclcar cell and highly purified B cell cultures. IgM-RF was synthesized after activation in cultures from healthy subjects and spontaneously in cultures from RA patients. In contrast to polyclonal IgM synthesis, IL-2 failed to augment IgM-RF synthesis in cell cultures from either healthy subjects or RA patients. This study demonstrates different effects of IL-2 on IgM and IgM-RF synthesis.
Clustering of neutrophil leucocytes in serum: possible role of Clq-containing immune complexes
Authors: STURFELT G , JONSSON H , HELLMER G , SJöHOLM A G 
Published: August 2010

SUMMARYClustering activity for neutrophil granulocytes was generated in pooled normal human serum (NHS) by incubation of the serum with preformed IgG aggregates, but not in heat-treated NHS (56°C, 30 min), indicating that the function was complement-dependent. Judging from results of experiments with complement-deficient sera, and serum depleted of Clq, factor D and properdin, recruitment of the complement system beyond Cl was not required for induction of the activity. Zymosan treatment of NHS resulted in some neutrophil clustering activity, but recombinant C5a had a limited effect. Clq added to heat-treated NHS in conjunction with preformed IgG aggregates supported neutrophil clustering in a dose-dependent manner. The serum Clq inhibitor, a chondroitin 4-sulphate proteoglycan known to interact with the collagenous part of Clq, clearly reduced neutrophil clustering in heat-treated NHS supplemented with Clq and IgG aggregates. The Clq inhibitor also reduced the inherent neutrophil clustering activity of some sera from patients with systemic lupus erythematosus (SLE). Neutrophil clustering activity in SLE serum was earlier shown to be inversely related to the number of circulating neutrophils in vivo. Although the precise mechanisms remain unclear, we propose that Clq-containing immunoglobulin complexes mediate neutrophil clustering through Clq receptors, and that this might contribute to pathogenesis of immune complex diseases such as SLE.
Trichosanthin, an initiator of the alternative complement activation pathway
Authors: CHEN X , MA B-L 
Published: August 2010

SUMMARYTrichosanthin (TCS), a protein purified from the plant Trichosanthes Kirilowii Maxim, activates normal human serum complement via the alternative pathway, as shown by TCS-induced C3 conversion in normal serum and its prevention by depletion of factor B, but not with the addition of EGTA. Injection of TCS to BALB/c mice consumed the complement alternative pathway (APC) activity in serum, implying in vivo activation of the alternative pathway by TCS. Elevation of peripheral blood leucocyte count as well as protein exudation and neutrophil accumulation in the peritoneal cavities could be induced by peritoneal injection of TCS. The main effect of complement activation by TCS was demonstrated to be induction of neutrophil accumulation.
Antibodies to the protein core of the small cell lung cancer workshop antigen cluster-w4 and to the leucocyte workshop antigen CD24 recognize the same short protein sequence leucine-alanine-proline
Authors: WEBER E , LEHMANN H P , BECK-SICKINGER A G , WAWRZYNCZAK E J , WAIBEL R , FOLKERS G , STAHEL R A 
Published: August 2010

SUMMARYWe recently described the identity of the small cell lung cancer (SCLC) cluster-w4 antigen and the human B cell differentiation marker CD24, a glycosylphosphatidylinositol (GPI)-anchored, highly glycosylated surface molecule of only 31–35 amino acids [15]. The specificities of three anti-cluster-w4 and of eleven anti-CD24 MoAbs have been investigated with respect to their binding capacity to the protein core of cluster-w4/CD24 antigen. Four overlapping peptides spanning this protein core were synthesized. MoAbs shown to bind to two overlapping peptides by antibody binding inhibition using the clustcr-w4/CD24-positive SCLC cell line SW2 and by direct peptide binding detected in an ELISA were investigated in more detail. To determine the exact epitopes recognized by these MoAbs, an epitope mapping assay using peptides synthesized onto polyethylene pins was established. The three anti-cluster-w4 MoAbs SWA11, SWA21 and SWA22 and the anli-CD24 MoAbs OKB2 and ALB9 recognized the same short leucine-alanine-proline (LAP) sequence in an area without potential glycosylation sites close to the GPI anchor of the protein core of the cluster-w4/CD24 antigen.