bluuebunny/crossref_metadata_2025_split huggingface dataset:
Alterations in the number of circulating leucocytes, phenotype of monocyte and cytokine production in patients undergoing cardiothoracic surgery
Authors: HIESMAYR M J , SPITTLER A , LASSNIGG A , BERGER R , LAUFER G , KOCHER A , ARTEMIOU O , BOLTZ-NITULESCU G , ROTH E 
Published: March 2003

SUMMARY
Changes in the differential blood cell count, monocyte phenotype and the cytokine plasma levels in a group of seven patients with cardiac surgery/cardiopulmonary bypass (CPB) and nine patients with thoracic surgery/without CPB, both receiving identical opioid-based anaesthetic technique, were assessed. A significant reduction in the number of circulating lymphocytes and monocytes was observed after anaesthesia and surgery. Interestingly, at the end of surgery as well as 1 day post-surgery a marked increase in the number of granulocytes was noted. General anaesthesia and surgery caused a significant reduction of HLA-DR and CD11c/CD18 molecules, starting immediately after induction of anaesthesia, and an increase of CD64 at day 1 after anaesthesia. The use of a CPB was followed by a significant reduction of CD32, CD16, CD54 and HLA-ABC antigens expression at the end of surgery. One day after surgery these parameters returned nearly to baseline values with the exception of CD54. A monocyte subpopulation, characterized by low CD14, high CD16 and HLA-DR expression (CD14+CD16+HLA-DR++) was found in both groups at each time point, and the percentage of this cell subset decreased from baseline to 24 h. The plasma concentrations of IL-6 and IL-10 increased considerably during CPB. No dynamic changes of IL-1 level due to surgery or CPB were found. We conclude that anaesthesia as well as the use of CPB induced profound alterations in the number of circulating leucocytes, and in the phenotype of monocyte and cytokine production.
Heat shock protein 70 (hsp70) as a major target of the antibody response in patients with pulmonary cryptococcosis
Authors: KAKEYA H , UDONO H , MAESAKI S , SASAKI E , KAWAMURA S , HOSSAIN M A , YAMAMOTO Y , SAWAI T , FUKUDA M , MITSUTAKE K , MIYAZAKI Y , TOMONO K , TASHIRO T , NAKAYAMA E , KOHNO S 
Published: March 2003

SUMMARYCryptococcus neoformans causes infection in individuals with defective T cell function, such as AIDS, as well as without underlying disease. It has been suggested that humoral as well as cellular immunity might play an important role in the immune response to C. neoformans infection. We have recently shown, using immunoblotting, that the 70-kD hsp family of C. neoformans was the major target molecule of the humoral response in murine pulmonary cryptococcosis. In this study we also used immunoblotting to define the antibody responses in the sera of 24 patients with pulmonary cryptococcosis: 21 proven and three suspected diagnoses. Anti-C. neoformans hsp70 antibody was detected in 16 of 24 (66.7%) patients with pulmonary cryptococcosis. Fourteen of 17 (82.3%) patients with high antigen titres (≥ 1:8) and two of seven (28.6%) patients with low titres (≤ 1:4) had detectable levels of anti-hsp70 antibody. Sera from patients positive for anti-hsp70 antibody showed high titres in the Eiken latex agglutination test for the detection of serum cryptococcal antigen. Our results indicate that the 70-kD hsp family from C. neoformans appears to be a major target molecule of the humoral response, not only in murine pulmonary cryptococcosis, but also in human patients with pulmonary cryptococcosis.
Disparate T cell requirements of two subsets of lupus-specific autoantibodies in pristane-treated mice
Authors: RICHARDS H B , SATOH M , JENNETTE J C , OKANO T , KANWAR Y S , REEVES W H 
Published: March 2003

SUMMARYIntraperitoneal injection of pristane induces a lupus-like disease in BALB/c and other non-autoimmune mice characterized by autoantibody production and the development of immune complex disease closely resembling lupus nephritis. Two subsets of autoantibodies are induced by pristane: IgG anti-DNA and -chromatin autoantibodies are strongly IL-6-dependent, whereas IgG anti-nRNP/Sm and -Su antibodies are not. The present studies were carried out to examine the role of T cells in establishing this dichotomy between the production of anti-nRNP/Sm/Su versus anti-DNA/chromatin autoantibodies. Autoantibody production and renal disease were evaluated in athymic (nude) mice treated with pristane. BALB/c nu/nu mice spontaneously developed IgM and IgG anti-single-stranded (ss)DNA and -chromatin, but not anti-nRNP/Sm or -Su, autoantibodies. Pristane treatment increased the levels of IgG anti-chromatin antibodies in nu/nu mice, but did not induce production of anti-nRNP/Sm or -Su antibodies. In contrast, BALB/c nu/+and +/+control mice did not spontaneously produce autoantibodies, whereas anti-nRNP/Sm and -Su autoantibodies were induced by pristane in approx. 50% of nu/+ and +/+mice and anti-DNA/chromatin antibodies at lower frequencies. Nude mice spontaneously developed mild renal lesions that were marginally affected by pristane, but were generally milder than the lesions developing in pristane-treated nu/+ and +/+mice. The data provide further evidence that two distinct pathways with different cytokine and T cell requirements are involved in autoantibody formation in pristane-induced lupus. This dichotomy may be relevant to understanding differences in the regulation of anti-DNA versus anti-nRNP/Sm autoantibodies in systemic lupus erythematosus, as well as the association of anti-DNA, but not anti-nRNP/Sm, with lupus nephritis.
Investigation of the expression of IL-1β converting enzyme and apoptosis in normal and inflammatory bowel disease (IBD) mucosal macrophages
Authors: McALINDON M E , GALVIN A , McKAIG B , GRAY T , SEWELL H F , MAHIDA Y R 
Published: March 2003

SUMMARYActivated mucosal macrophages are derived from circulating monocytes and appear to play a major role in the pathogenesis of IBD. We have recently shown that IBD, but not normal, mucosal macrophages express the active form of IL-1β converting enzyme (ICE) and are therefore capable of releasing mature IL-1β. ICE expression by other mucosal cell types is unknown. Active ICE expression has also been implicated in apoptosis. The aim of this study was to investigate ICE expression (using an antibody that recognizes both active and precursor forms) in normal and IBD mucosa and to determine whether ICE-expressing macrophages are undergoing apoptosis. Normal and active IBD mucosal cells, in tissue sections and after isolation, were studied by immunohistochemistry and flow cytometry. In the mucosa, macrophages were the predominant ICE-expressing cell type. In contrast to normal, most IBD mucosal macrophages expressed ICE. Of IBD colonic macrophages 11.8 ± 3.2%, and of normal colonic macrophages 6.6 ± 0.6% expressed Apo2.7, a marker for apoptotic cells. Similar data were obtained when annexin V was used to identify cells undergoing apoptosis. DNA fluorescence flow cytometric analysis of normal and IBD lamina propria cells showed the presence of only small hypodiploid DNA peaks. We conclude that in the human intestinal mucosa, macrophages are the predominant ICE-expressing cell type. Expression of the active form of ICE and macrophage apoptosis are not interdependent. One mechanism of loss of resident macrophages from normal mucosa and of recruited macrophages from IBD mucosa is by apoptosis.
Inhibition of apoptosis by ionomycin and zinc in peripheral blood mononuclear cells (PBMC) of leprosy patients
Authors: GUPTA A , SHARMA V K , VOHRA H , GANGULY N K 
Published: March 2003

SUMMARYPBMC from tuberculoid (BT/TT) and lepromatous leprosy (BL/LL) leprosy patients showed spontaneous apoptosis when cultured in the absence of mitogen for 24 h, which was inhibited by anti-tumour necrosis factor-alpha (TNF-α) antibodies. Apoptosis was also inhibited by ionomycin and zinc, which also increased IL-2 and decreased TNF-α production. The increase in IL-2 production suggests a mechanism whereby dietary supplements with zinc might alter the cell-mediated immunity response in leprosy patients.
Comparison of enterovirus-specific cellular immunity in two populations of young children vaccinated with inactivated or live poliovirus vaccines
Authors: JUHELA S , HYÖTY H , UIBO R , MERISTE S H , UIBO O , LÖNNROT M , HALMINEN M , SIMELL O , ILONEN J 
Published: March 2003

SUMMARYEnterovirus-specific cellular immunity was studied in Estonian and in Finnish children at the age of 9 months. The aim was to evaluate the level of responsiveness in two neighbouring countries with different poliovirus immunization practices and striking differences in the incidence of insulin-dependent diabetes mellitus (IDDM), a disease in which early enterovirus infections are an aetiological risk factor. The Estonian children immunized with live attenuated polio vaccine had stronger T cell responses to coxsackievirus B4 and poliovirus type 1 when compared with Finnish children immunized with inactivated polio vaccine (median stimulation indices 10.4 and 6.3 in Estonian children and 1.9 and 2.9 in Finnish children, respectively; P &lt; 0.05). Lymphocytes stimulated by poliovirus type 1 antigen expressed interferon-gamma (IFN-γ) mRNAs, which strongly correlated with the level of proliferation responses. Lymphocytes of Estonian children had a tendency towards stronger expression of IFN-γ upon poliovirus challenge when compared with Finnish children. The number of children who had experienced coxsackievirus B infections, as determined by the presence of neutralizing antibodies, did not differ between Estonian and Finnish children. The results show that Finnish children have weaker cellular immunity against enteroviruses at the age of 9 months compared with Estonian children at the same age. This is most probably due to the difference in polio vaccination schedules; in Estonia live poliovirus vaccine is used and given at earlier ages than the inactivated vaccines in Finland. This leads to stronger T cell immunity which cross-reacts with other enterovirus serotypes. This may explain the lower incidence of IDDM in Estonia by providing effective protection against diabetogenic enterovirus strains in Estonian children.
Nickel-induced proliferation of both memory and naive T cells in patch test-negative individuals
Authors: Lisby S , Hansen L H , Menné T , Baadsgaard O 
Published: March 2003

SUMMARYLymphocyte transformation test has often been used as an in vitro test for nickel allergy. We have previously demonstrated the presence of nickel-reactive T cells in individuals with no history of allergic disease and with a negative patch test towards NiSO4. In this study, we show that this proliferative response was mainly confined to T cells within the CD4+ subset. In contrast to conventional recall antigens such as tetanus toxoid, in vitro stimulation using NiSO4 activated both FACS-purified CD4+CD45RA+‘naive’ and CD4+CD45RO+‘memory’ T cells. To determine which cell population reacted with nickel to induce T cell activation, peripheral blood mononuclear cells were separated into macrophages and non-adherent, HLA-DR-depleted T cells. We found that preincubation of monocytes/macrophages but not T cells with NiSO4 resulted in subsequent T cell proliferation. This result demonstrated that nickel did not exhibit any direct effect on the T cell. Furthermore, the NiSO4-induced T cell proliferation could be blocked by antibodies towards MHC class II (HLA-DR) molecules. Our results substantiate the concept that individuals with a negative patch test towards NiSO4 contain in their peripheral blood T cells capable of recognizing nickel or nickel-modified peptides. In contrast to conventional recall antigens, both memory and naive T cells were activated. Thus, when compared with data obtained from nickel-allergic individuals, this study shows a comparable nickel-inducible T cell activation in non-allergic individuals.
Progressive polarization towards a T helper/cytotoxic type-1 cytokine pattern during age-dependent maturation of the immune response inversely correlates with CD30 cell expression and serum concentration
Authors: Krampera M , Vinante F , Tavecchia L , Morosato L , Chilosi M , Romagnani S , Zanolin M E , Pizzolo G 
Published: March 2003

SUMMARYIn order to investigate the T cell cytokine profile during age-dependent maturation of the immune response, we evaluated the cytokine expression of CD4+ and CD8+ circulating cells by flow cytometric single-cell analysis after non-specific stimulation in vitro in different age groups of normal individuals, from cord blood to adulthood. Moreover, we correlated these lymphocyte cytokine patterns with the expression/release of CD30, a member of the tumour necrosis factor (TNF) receptor superfamily, which has been suggested to be related to the T helper/cytotoxic (Th(c))2-type immune responses, in order to verify this association in vivo, in non-pathological conditions. The results showed a progressive increase of circulating Th(c)1-type, interferon-gamma (IFN-γ)- and/or IL-2-producing T cells along with ageing and, conversely, a stable number, although higher than in cord blood samples, of CD4+/IL-4+ T cells in the post-natal groups. In addition, serum levels of soluble CD30 (sCD30) and numbers of circulating CD4+/CD30+ and CD8+/CD30+ T cells were significantly higher in children aged &lt; 5 years in comparison with those found either in cord blood or in blood from both older children and adults. These data support the concept of a progressive polarization of the Th(c) cell cytokine profile towards the Th(c)1 pattern during age-dependent maturation of the immune response. Moreover, the peak of CD30 expression/release in early infancy before the Th(c)1 shifting occurs, although not associated with a significant increase of circulating IL-4+ T cells, raises the question of the possible relationship in vivo between CD30 and Th(c)2-type immune responses.
Isotype distribution and clinical relevance of anti-β2-glycoprotein I (β2-GPI) antibodies: importance of IgA isotype
Authors: Lakos G , Kiss E , Regéczy N , Tarján P , Soltész P , Zeher M , Bodolay E , Szakony Sz , Sipka S , Szegedi Gy 
Published: March 2003

SUMMARYThe aim of this study was to evaluate the prevalence of IgG, IgA and IgM anti-β2-GPI antibodies in anti-phospholipid syndrome (APS), and to establish the clinical significance of IgA type antibodies compared with the other isotypes. Anti-β2-GPI antibodies were measured in the sera of 70 patients by solid-phase enzyme immunoassay in γ-irradiated polystyrene plates coated with human purified β2-GPI. Thirty-three out of the 70 patients were classified as having APS: three of them had primary, and 30 had secondary APS related to systemic lupus erythematosus (SLE). The remaining 37 patients had SLE without APS. Anti-β2-GPI antibodies of IgG, IgA and IgM isotypes were present in 84.8%, 59.3% and 51.5% of patients with APS. Both the frequency and the level of each isotype were significantly higher in patients with APS. This association was very strong for IgA (P = 0.0004 for the antibody frequency and P &lt; 0.0001 for the antibody level), as well as for IgG type antibodies (P &lt; 0.0001 and P &lt; 0.0001), whereas it was weaker for IgM (P = 0.01 and P = 0.04). A strong relationship was demonstrated between increased IgA anti-β2-GPI antibody levels and a history of venous thrombosis, thrombocytopenia, heart valve disease, livedo reticularis and epilepsy. IgG anti-β2-GPI antibodies were associated with the presence of lupus anticoagulant (LA) in addition to the main features of APS. However, antibodies of IgM isotype were related only to thrombocytopenia and heart valve disease. We recommend the evaluation of anti-β2-GPI antibodies of IgA isotype in addition to IgG in patients with clinical suspicion of APS.
Perforin and Fas/Fas ligand-mediated cytotoxicity in acute and chronic woodchuck viral hepatitis
Authors: Hodgson P D , Grant M D , Michalak T I 
Published: March 2003

SUMMARYThe Fas ligand (FasL)/Fas and the perforin-granzyme cytotoxic pathways presumably play a central role in the development of hepatocellular injury in viral hepatitis. To recognize the potential contribution of FasL and perforin-based cell killing in hepadnaviral infection, we adopted a cytotoxic assay using murine Fas+ P815 and human Fas− K562 cells as targets. Freshly isolated peripheral blood mononuclear cells (PBMC) from woodchucks with newly acquired woodchuck hepatitis virus (WHV) infection (n = 6), with chronic WHV hepatitis (n = 9), and from healthy animals (n = 11) were used as effector cells. We have found that woodchuck lymphoid cells kill cell targets via both the FasL/Fas and the perforin death pathways. The contribution of Fas-dependent cytolysis was ascertained in blocking experiments with anti-Fas antibody and by incubation of PBMC with cyclohexamide to prevent de novo synthesis of FasL. The involvement of the perforin pathway was confirmed by treatment of K562 cells with colchicine to inhibit the microtubule-dependent perforin release. Comparative analysis showed that peripheral lymphoid cells from acute WHV hepatitis, but not those from chronic WHV infection, are more cytotoxic and that this increase seems to be entirely due to activation of perforin-mediated killing. The data indicate that acute infection in woodchucks is associated with the augmented capacity of lymphoid cells to elicit perforin-dependent killing, but in chronic infection, independent of the severity of liver disease and duration of chronicity, these cells have the same or lower cytotoxic potential as PBMC from healthy controls. These findings suggest a role for non-specific cellular immunity, presumably natural killer (NK) cells, in the control of early WHV infection and in the progression of chronic hepatitis.
The effect of site-specific monoclonal antibodies directed to toxic shock syndrome toxin-1 in experimentalStaphylococcus aureusarthritis
Authors: Verdrengh M , Kum W , Chow A , Tarkowski A 
Published: March 2003

SUMMARYStaphylococcus aureus produces a large number of potential virulence factors, among these the superantigen toxic shock syndrome toxin-1 (TSST-1). We have recently demonstrated that TSST-1 is involved in the pathogenesis of septic arthritis. Recent data show that the TSST-1 molecule is composed of two distinct domains, one proposed to interact with T cell receptor (TCR) and one with the MHC class II. The aim of this study was to assess if interaction between TSST-1-specific MoAbs directed to sites on the MHC and/or TCR Vβ affects the development of experimental S. aureus-induced arthritis. For that purpose we used a panel of seven MoAbs, which were injected intraperitoneally before and after inoculation with a TSST-1-producing S. aureus strain. Administration of antibodies did not affect the development of arthritis, suggesting inefficacy of such a procedure in neutralization of exotoxin-mediated disease manifestations.
Intercellular adhesion molecule-1 (ICAM-1) deficiency protects mice against severe forms of experimentally induced colitis
Authors: Bendjelloul F , Malý P , Mandys V , Jirkovská M , Prokešová L , Tučková L , Tlaskalová-Hogenová H 
Published: March 2003

SUMMARYICAM-1 (CD54), the ligand for LFA-1 and Mac-1, is up-regulated during inflammatory reaction on the activated vascular endothelium. To determine its role in intestinal inflammation, we induced acute experimental colitis in mice with a deleted ICAM-1 gene, by feeding them with 3% dextran sodium sulphate (DSS) in drinking water for 7 days. Chronic colitis was elicited by DSS similarly, followed by 2 weeks with water. In the acute phase of inflammation, ICAM-1-deficient mice exhibited a significantly lower mortality rate (5%) than control C57Bl/6J mice (35%). Control animals, but not the ICAM-1-deficient mice, exhibited diarrhoea and rectal bleeding. Histological examination of large-bowel samples evaluated the intensity of inflammatory changes, and type and extent of mucosal lesions. In the acute phase, 33.3% of samples from ICAM-1-deficient mice exhibited mucosal defects (flat and fissural ulcers), predominantly mild to moderate inflammatory infiltrate within the lamina propria mucosae and lower grades of mucosal lesions. Much stronger inflammatory changes were present in control animals, flat ulcers (sometimes multiple) and fissural ulcers being observed in 62.5% of samples. Mucosal inflammatory infiltrate was moderate to severe, typically with higher grades of mucosal lesions. In chronic colitis, smaller inflammatory changes were found in the large bowel. The two mouse strains differed, the chronic colitis being accompanied by an increased serum level of anti-epithelial IgA autoantibodies in C57Bl/6 control mice but not in ICAM-1-deficient mice. These findings provide direct evidence of the participation of ICAM-1 molecule in the development of experimentally induced intestinal inflammation.
Long-term persistence of oligoclonal serum IgM repertoires in patients treated with allogeneic bone marrow transplantation (BMT)
Authors: Näsman Björk I , Brissac C , Remberger M , Mattsson J , Klaesson S , Ringdén O , Stewart J , Lundkvist I 
Published: March 2003

SUMMARY
Immunoglobulin gene rearrangements in patients treated with BMT have restricted repertoire diversity. Clonal variability remains low for 3 months and reconstitution of the humoral immune system appears to follow a wave-like pattern. In the present study we analysed serum IgM and IgG repertoires in 44 patients from 1 week to 3 years after transplantation. We applied a quantitative immunoblot technique in combination with a newly developed method for estimation of repertoire diversity in complex mixtures of antibodies. Our results demonstrate that 60% of BMT patients have severely reduced diversity in the IgM repertoire during and after the first year post-BMT, compared with healthy controls. In contrast, the majority of patients have a polyclonal IgG repertoire, similar to that of healthy controls. Serum IgM repertoires remain oligoclonal even though the serum concentration of total IgM is within normal range around 6 months post-BMT. During the first years after transplantation IgM as well as IgG repertoires are less diverse in patients receiving a BM graft from a sibling donor compared with those receiving a graft from an HLA-matched unrelated donor. Patients in the latter group show a higher incidence of infections and minor antigen mismatches which may promote the development of a diverse immunoglobulin repertoire post-BMT.
Blister fluid T lymphocytes during toxic epidermal necrolysis are functional cytotoxic cells which express human natural killer (NK) inhibitory receptors
Authors: Le Cleach L , Delaire S , Boumsell L , Bagot M , Bourgault-Villada I , Bensussan A , Roujeau J C 
Published: March 2003

SUMMARYToxic epidermal necrolysis (TEN) is a rare life-threatening adverse drug reaction characterized by a massive destruction of the epidermis. Immunohistological studies of skin biopsies of TEN showed infiltrates of predominantly CD8+ T lymphocytes even though other authors reported a prominent involvement of cells of the monocyte-macrophage lineage. The aim of this study was to characterize phenotypically and functionally the cells present in the cutaneous blister fluid of four patients with TEN. We first determined that lymphocytes were predominant in blister fluid obtained early, while monocytes/macrophages later became the most important population. We then showed that this lymphocyte population, mainly CD3+CD8+, corresponded to a peculiar cell subset as they expressed cutaneous leucocyte antigen, killer inhibitory receptors KIR/KAR and failed to express CD28 molecule. Functionally, we determined that blister T lymphocytes had a cytotoxic T lymphocyte (CTL)- and NK-like cytotoxicity. The role of this cytotoxic lymphocyte population present at the site of lesions during TEN remains to be understood.