bluuebunny/crossref_metadata_2025_split huggingface dataset:
HLA expression in hepatocellular carcinoma cell lines
Authors: WADEE A A , PATERSON A , COPLAN K A , REDDY S G 
Published: July 2010

SUMMARYThe present study undertook to investigate the biological significance of human leucocyte antigen expression in hepatocellular carcinoma and to elucidate the role of potential modulating agents on human leucocyte antigen expression. These studies used several hepatic tumour-derived cell lines as in vitro model systems. The cell lines included PLC/PRF/5 (Alexander cell line), Hep3B. HepG2, TONG PHC, HA22T/VGH, HA59T/VGH and Mahlavu, The cell lines K562 and Raji were used as negative and positive controls, respectively. K562, a B tymphoid-derived cell line, was shown to express negligible amounts of human leucocyte anligens, while Raji, an erythromyeloid-derived cell line, expressed both class I and class II human leucocyte anligens as well as their respective invariant chains, β2-niicroglobulin and Ii. Using an ELISA, experiments performed on these cell lines confirmed the natural expression of class I and class II antigens by the HA22T/VGH and HA59T/VGH cell lines, whereas PLC/PRF/5 displayed class II surface antigens only. The effects of modulating agents such as interferon-gamma sodium bulyrate and clofazimine on human leucocyte antigen expression were investigated using the HA22T/VGH, HA59T/VGH and TONG PHC cell lines. These agents increased class 1 and class II human leucocyte antigen expression on HA22T/VGH and TONG PHC cells, but had no effect on the HA59T/VGH cell line. The results suggest a potential use for these agents as modulators of human leucocyte antigen expression by human heptocellular cell lines.
Study of IL-2 receptor expression after chemoimmunotherapy in patients treated for metastatic malignant melanoma
Authors: MOUAWAD R , ICHEN M , RIXE O , BENHAMMOUDA A , VUILLEMIN E , WEIL M , KHAYAT D , SOUBRANE C 
Published: July 2010

SUMMARYUsing flow cytometry, cellular IL-2 receptors were studied before and following chemoimmunotherapy combination in 20 patients with metastatic malignant melanoma (MMM). Patients received cisplatin (100 mg m2) at days 1 and 28, recombinant IL-2 by continuous infusion from days 3 to 6, 17 to 21, 31 to 34, and 45 to 49. Interferon-alpha (IFN-α) was given subcutaneously three times weekly. In terms of clinical response, we observed 55% objective response (complete: 15%), When pretreatment blood samples were compared with those of healthy donors, we did not observe any change in low (α chain) and high affinity receptor (α+β) expression. In contrast, intermediate affinity p75 (β chain) expression was decreased significantly (P ≤ 0.0001) in MMM patients. During treatment, we found a dramatic increase of β chain as well as high affinity (α+β) expression in responding patients, as soon as IL-2 therapy began. Furthermore, the increase of β chain expression was limited to natural killer (NK) cells (CD56+). In non-responding patients, on the other hand, increase of both receptors was seen only at day 31. These data suggest the involvement of β chain expression in the mechanism of cell activation after chemoimmunotherapy. Moreover, this early 3 chain expression is correlated with the clinical response to chemoimmunotherapy.
Anti-lymphocyte antibodies in plasma of HIV-1–infected patients preferentially react with MHC class Il-negative T cells and are linked to antibodies against gp41
Authors: MÜLLER C , KUKEL S , SCHNEWEIS K E , BAUER R 
Published: July 2010

SUMMARYIt has previously been shown that HIV-infected patients develop anti-lymphocyte antibodies. The relationship between anti-lymphocyte antibodies and antibodies against different viral antigens is unknown, and it remains controversial whether some lymphocyte subpopulations are targeted preferentially. We have set out using three-colour flow cytometry to measure antibodies against different lymphocyte subsets. Staining with anti-human immunoglobulin and two MoAbs was performed to characterize the immunoglobulin toad of different lymphocyte subsets. Comparison was done between patients'antibody reactivity against HlV-1 antigens and anti-lymphocyte antibodies. We were able to demonstrate the presence of anti-lymphocyte antibodies in approximately 75% of the HIV-infected patients (n = 78) (healthy controls were all negative). MHC class Il-negative T cells showed a stronger reaction with anti-lymphocyte antibodies than B cells or MHC class Il-positive T cells. Patients with antibodies against CD4 lymphocytes showed a significantly higher antibody reaction with the retroviral antigen gp41 than patients without these antibodies. An association between anti-lymphocyte antibodies and antibody reactivity against other HIV-1 antigens was not noticed. In conclusion, anti-lymphocyte antibodies in HIV-1-infected patients show a preferential reactivity with T cells which lack expression of MHC class II molecules. There is an increased antibody reactivity against gp41 in patients with anti-CD4+ T cell antibodies. The association hints at a specific origin of anti-lymphocyte antibodies in HIV-1-infected patients due to cross-reactivity with viral epitopes or network phenomena. These anti-CD4 cell antibodies could be of interest in the clinical course of HIV infection.
Induction of multinucleated giant cells from rheumatoid arthritis (RA) synovial adherent cells by anti-DR antibody
Authors: MATSUYAMA T , NAKASHIMA N , MATSUDA T , NAKAMURA H , UCHIDA S , ABE T 
Published: July 2010

SUMMARYTo determine the effects of signalling through the DR molecule on synoviocytes from RA patients, the synovial adherent cells were incubated with anti-DR antibodies. After 24 h incubation, we found the formation of multinucleated giant cells in that culture. These multinucleated giant cells showed characteristics of monocyte-macrophage lineage cells and precursor of osteoclasts. Cyclohexamide inhibited the formation of multinucleated giant cells, but not the aggregation of synovial cells, suggesting that newly synthesized proteins are associated with the cell fusion. These results revealed a new mechanism in multinucleated giant cell formation.
Isolation and characterization of migratory human skin dendritic cells
Authors: RICHTERS C D , HOEKSTRA M J , VAN BAARE J , DU PONT J S , HOEFSMIT E C M , KAMPERDIJK E W A 
Published: July 2010

SUMMARYA method is described to isolate and characterize human skin dendritic cells (DC). This method is based on the migratory capacities of these cells. The cells migrated “spontaneously” out of split-skin explants into the medium during a 24-h culture period and contained up to 75% CD1a+ cells. After removal of co-migrated T cells and macrophages, the highly enriched (&gt;95% CD1a*) DC showed potent allo-antigen-presenting capacities. About 25% of the CD1a+ cells were also positive for the dermal DC marker CD1b, whereas only 15-20% of the cells contained Birbeck granules, the characteristic cell organelle of the epidermal Langerhans cell. Before culture. CD1a* DC were observed on cryostat sections not only in the epidermis but also in the dermis. After culture, the number of CD1a+ cells in both epidermis and dermis had decreased. Not all the cells had migrated during the culture period; some CD1a+ cells could still be detected in the epidermis and dermis after culture. Thus, using this method, potent allo-stimulating CD1a+ cells, migrating from both epidermis and dermis can be obtained without the use of enzymes.
Common variable immunodeficiency (CVID) and MxA-protein expression in blood leucocytes
Authors: RUMP J A , JAKSCHIESS D , WALKER U , SCHLESIER M , VON WUSSOW P , PETER H H 
Published: July 2010

SUMMARYThe underlying immunopathogenic mechanism of CVID has been suspected to involve a chronic viral infection or an autoimmune condition. However, formal proof of viral infection is lacking. Measurement of MxA-protein in leucocyte lysates is a sensitive test for evaluating the activation of the host's interferon system. Both viral infections and autoimmune diseases such as systemic lupus erythematosus (SLE) strongly induce MxA-protein in peripheral leucocytes. We therefore examined 15 patients with longlasting hypogammaglobulinaemia for MxA-protein induction in vivo: 13 patients suffered from CVID, one from hyper-IgM syndrome, and one patient had chronic B lymphocytic leukaemia associated with immunoglobulin deficiency and chronic papilloma virus infection (condylomata accuminata). Only the latter patient exhibited a strong MxA-protein expression; two CVID patients were borderline positive, and the remaining 12 patients including the hyper-IgM syndrome were MxA-protein-negative. There was no relationship between MxA expression and low CD4/CD8 ratios or increased CD8/CD57+ T cell counts, although both conditions are often observed in CVID as well as in chronic viral infections. When exposed in vitro to interferon-alpha (IFN-α), peripheral blood leucocytes of four MxA-negative patients were capable of producing normal amounts of MxA-protein. Taken together, these results argue against a viral or autoimmune pathogenesis of CVID.
Technical Report: results of immunological tests on faecal extracts are likely to be extremely misleading
Authors: Ferguson A , Humphreys K A , Croft N M 
Published: July 2010

SUMMARY
Clinical investigation of gut immunity is difficult because of the need to study intestinal tissues or secretions directly. Others have reported that immunoglobulins, antibodies and cytokines can be detected in saline extracts of faeces. We have assessed the validity of this approach by measuring immunoglobulins, albumin, α1-antitrypsin and isotype-specific antibodies in matched samples of faeces and whole gut lavage fluid. Results were compared as estimated output per day, and by using haemoglobin as a common reference substance. Samples were obtained from 10 patients with active inflammatory bowel disease and 10 with other benign GI diseases. For immunoglobulins, albumin and antibodies, the amount detected in faeces varied from &lt; 0.01% to 35.5% (based on estimated daily output) and &lt; 0.01 % to 18.5% (based on haemoglobin) of the amount known to be produced in the gut from results of assays on whole gut lavage fluid (WGLF); there were significantly higher rates of recovery in faecal specimens from patients with active gut inflammation than from other patients. Detection rates and titres of specific antibody in faeces were even lower than those for immunoreactive IgA. These data indicate that immunological tests on saline extracts of faeces do not represent the true status of the gut humoral immune system, and such studies should be strongly discouraged.
Differing antibody IgG isotypes in the polar forms of leprosy and cutaneous leishmaniasis characterized by antigen-specific T cell anergy
Authors: ULRICH M , RODRIGUEZ V , CENTENO M , CONVIT J 
Published: July 2010

SUMMARYLeprosy and American cutaneous leishmaniasis are tropical diseases which present a spectrum of clinical and immunological manifestations. Lepromatous leprosy and diffuse cutaneous leishmaniasis are the severe, progressive polar forms of disease characterized by persistent T cell anergy. Relative concentrations of antibodies belonging to the four IgG isotypes have been determined in these forms of disease as well as active visceral leishmaniasis, which presents transitory T cell anergy. Leishmania-specific lgG4 antibodies predominated in 19/20 sera from patients with diffuse cutaneous leishmaniasis, and IgG1 antibodies predominated in 9/10 cases of untreated visceral leishmaniasis. The predominant IgG isotype of Mycobacterium leprae-specific antibodies in untreated lepromatous leprosy was remarkably variable (IgG1, igG2, IgG3 and IgG4 in 8, 6, 2 and 1 sera, respectively). Differing IgG antibody isotypes have been associated with distinct CD4+ T cell helper subpopulations and their characteristic lymphokine profiles in several pathologies. These results suggest that T cell anergy in chronic intracellular infections may be associated with as yet undefined mechanisms which modulate reported T helper cell lymphokine isotype relationships.
Antibodies to small ribonucleoprotein and to 73-kD heat shock protein: two distinct markers of mixed connective tissue disease
Authors: APPELBOOM T , KAHN M F , MAIRESSE N 
Published: July 2010

SUMMARYWe set out to discover whether antibodies to small ribonucleoprotein antigens (RNP) and to 73-kD heat shock protein (hsp 73) which have been proposed as markers of mixed connective tissue disease (MCTD) recognize different epitopes. MCTD serum was immunoadsorbed on hsp 73-coupled Sepharose and the affinity retained, and non-retained fractions were checked by immunoblotting for recognition of either purified bovine hsp 73 or calf thymus extract RNPs. The hsp 73 affinity-bound serum fraction recognized hsp 73 but not RNP antigens, the reverse being true for the non-retained fraction. We conclude that anti-hsp 73 and anti-RNPs are distinct markers of MCTD.
Interactions and molecular structure of cardiolipin and β2-glycoprotein 1 (β2-GP1)
Authors: Borchman D , Harris E N , Pierangeli S S , Lamba O P 
Published: July 2010

SUMMARYβ2-GP1 is a serum protein which influences binding of anticardiolipin antibodies to cardiolipin, may influence induction of these antibodies in animals and may play a role in anticardiolipin-mediated thrombosis. Various investigators have proposed that when β2-GP1 binds cardiolipin, structural alterations occur in one or both molecules, resulting in exposure of new epitopes for anticardiolipin binding, but there has been no proof that such alterations occur. Utilizing Fourier transform infrared spectroscopy, this study analysed the structure of cardiolipin and β2-GP1 alone, then mixed with each other. For pure cardiolipin, analysis of the CH2 stretching, scissoring and carbonyl bands suggested this molecule assumes a hexagonal crystal lattice packing structure in both anhydrous and aqueous samples. Based on the second derivative analysis of the amide 1 band from the β2-GP1 protein backbone, as well as Fourier self-deconvolution and curve fit algorithms, β2-GP1 was calculated to contain 18% turns, 37%α-helix, and 45%β-sheet structure. β2-GP1 binding with cardiolipin results in a significant change in the conformation as well as geometry of the lipid and protein components. This is indicated by a broadening of the CH stretching band and a marked shift in intensity of the carbonyl band of cardiolipin, indicating less hydrogen bonding. There was a decrease in β-sheet structure of β2-GP1 from 46% to 23% and appearance of 26% to 28% random structure. These findings indicate that mixing β2-GP1 with cardiolipin results in profound changes in both molecules which might explain the effect of β2-GP1 on anticardiolipin binding activity.
Differential alterations in plasma colony-stimulating factor concentrations in meningococcaemia
Authors: Waring P M , Presneill J , Maher D W , Layton J E , Cebon J , Waring L J , Metcalf D 
Published: July 2010

SUMMARYTo determine whether circulating levels of any of the cotony-stimulating factors (CSF) might contribute to the host response in severe sepsis, plasma concentrations of granulocyte CSF (GCSF), granulocyte-macrophage CSF (GM-CSF), and macrophage CSF (M-CSF), were measured by immunoassays in 20 subjects with meningococcaemia, a bloodstream infection caused by Neisseria meningitidis, that has proven to be a valuable model to study the responses of other inflammatory mediators during sepsis and septic shock in humans. Plasma G-CSF concentrations were transiently elevated in most subjects during the early phase of meningococcaemia, and were higher in subjects with septic shock (mean ± s.d. = 165± 142 ng/ml, n = 9) compared with those who remained normotensive (mean ± s.d.=7±2ng/ml, ng/ml, n=10) (p&lt;005). Peak plasma G-CSF concentrations &gt;10ng/ml were associated with the development of septic shock (P&lt;0.01), disseminated intravascular coagulation (p&lt;0.01). fulminant infection (P&lt;0.05), and a fatal outcome (p&lt;0.01). Plasma GM-CSF concentrations &gt; 1 ng/ml were briefly present in subjects with life-threatening septic shock (1–15 ng/ml, n = 5). and were strongly associated with fulminant meningococcaemia (P &lt;0.01). Plasma M-CSF concentrations were marginally elevated in all subjects, but were not associated with complications related to or arising from sepsis-induced organ injury. This study demonstrates that plasma levels of G-CSF, GM-CSF and M-CSF show very different responses during meningococcaemia, changes which presumably reflect the different roles played by these mediators in sepsis and, potentially, in septic shock.
Anti-malaria antibody-producing B cell frequencies in adults after aPlasmodium falciparumoutbreak in Madagascar
Authors: Migot F , Chougnet C , Henzel D , Dubois B , Jambou R , Fievet N , Deloron P 
Published: July 2010

SUMMARYThe central highlands of Madagascar offer a unique opportunity to explore the malaria immune memory, as the last murderous epidemic in the study area occurred 8 years ago. Quantification of the circulating memory B lymphocytes reacting to Plasmodium falciparum was assessed among 14 Madagascans by using a limiting dilution assay, applied to the EL4 culture system, which leads to activation, proliferation and differentia lion into antibody-secreting cells (ASC) of most peripheral B cells. This system allowed us to observe, without any malaria-specific restimulalion, a geometric mean frequency of one anti-P. falciparum ASC among 2992 circulating B cells, except for one Madagascan who did not have any detectable ASC. A geometric mean frequency of one anti-P. falciparum ASC among 1403 was obtained for six malaria hyperimmune Cameroonians, but conversely, no anti-malaria ASC was detected in the blood of six malaria non-immune French control subjects. Anti-P. falciparum ASC frequencies and serum specific antibodies were strongly related. Our results indicate that anti-malaria ASC are still present in peripheral blood of Madagascan subjects, who have not been exposed to P. falciparum for several years. These responder B cells reflect the malaria B cell memory acquired during the last epidemic.
Genetic variation in neutrophil accumulation in mice is not mediated through immigrant regulatory cells
Authors: Marley S B , Hadley C L , Wakelin D 
Published: July 2010

SUMMARYGenetic variation of induced peritoneal neutrophilia in mice was accompanied by parallel variation in macrophage responses. The timing of the macrophage responses in high responder (C57B1/10) mice indicated a potential role for these cells in mediating the enhanced neutrophil response. However, adoptive transfer of inflammatory macrophages did not induce neutrophilia. Analysis of peritoneal cytokine levels in high and low responder mice further indicated [hat IL-1, IL-3, GM-CSE, G-CSE and interferon-gamma (IFN-γ) were not involved in mediating the genetic variation observed. Exogenous tumour necrosis factor-alpha (TNF-α) was effective in inducing the high responder phenotype, despite the absence of detectable TNF-α in either peritoneal fluid or serum. A role for genetically determined differential expression of endothelial adhesion molecules in high and low responders is suggested.
Impaired dendritic cell functions because of depletion of natural killer cells disrupt antigen-specific immune responses in mice: restoration of adaptive immunity in natural killer-depleted mice by antigen-pulsed dendritic cell
Authors: Yoshida O , Akbar F , Miyake T , Abe M , Matsuura B , Hiasa Y , Onji M 
Published: July 2010

Summary
The primary aim of this study was to evaluate the role of natural killer (NK) cells on antigen-specific adaptive immune responses. After analysing the mechanism of impaired adaptive immune responses of NK-depleted mice, an immune interventional approach was developed to restore adaptive immunity in NK-depleted mice. NK cells were depleted from mice by administration of anti-asialo GM1 antibody (100 μl/mouse), twice, at an interval of 48 h. Hepatitis B surface antigen (HBsAg) was administered intraperitoneally to normal C57BL/6 mice (control mice) and NK-depleted mice. The levels of antibody to HBsAg (anti-HBs) in the sera and HBsAg-specific lymphocytes in the spleen were assessed. The functions of T lymphocytes, B lymphocytes and dendritic cells (DCs) were evaluated in vitro. HBsAg-pulsed DCs were prepared by culturing spleen DCs with HBsAg for 48 h and administered once to NK-depleted mice. The levels of anti-HBs in the sera and HBsAg-specific lymphocytes were significantly lower in NK-depleted mice compared with control mice (P &lt; 0·05). The functions of T and B lymphocytes were similar between control mice and NK-depleted mice. However, the functions of spleen DC and liver DC were significantly lower in NK-depleted mice compared with control mice (P &lt; 0·05). Administration of HBsAg-pulsed DCs, but not HBsAg, induced HBsAg-specific humoral and cellular immune responses in NK-depleted mice. Our study suggests that cross-talk between NK cells and DCs regulates the magnitude of adaptive immunity. In addition, antigen-pulsed immunogenic DCs represent potent immune modulator even if subjects with diminished innate immunity.
Two-dimensional gel electrophoresis analysis in simultaneous influenza pneumonia and bacterial infection in mice
Authors: Kosai K , Seki M , Yanagihara K , Nakamura S , Kurihara S , Imamura Y , Izumikawa K , Kakeya H , Yamamoto Y , Tashiro T , Kohno S 
Published: July 2010

Summary
Severe pneumonia is found in simultaneous influenza pneumonia and bacterial infection, and suggests a relationship with immunological mechanisms. Here, we performed two-dimensional gel electrophoresis to detect immunological molecules related to the fulminant pneumonia caused by influenza virus and Streptococcus pneumoniae co-infection in mice. We found two spots that were expressed strongly in co-infected mouse lungs, compared with S. pneumoniae or influenza virus singly infected mouse lungs. The spots were analysed by mass spectrometry, and identified as alpha-1 anti-trypsin (A1AT), known as an anti-protease for neutrophil-derived proteolytic enzymes, and creatine kinase, which reflects a greater degree of lung damage and cell death. A1AT expression was increased significantly, and proteolytic enzymes from neutrophils, such as neutrophil elastase, myeloperoxidase and lysozyme, were also secreted abundantly in influenza virus and S. pneumoniae co-infected lungs compared with S. pneumoniae or influenza virus singly infected lungs. These data suggest that A1AT may play a central role as a molecule with broad anti-inflammatory properties, and regulation of the neutrophil-mediated severe lung inflammation is important in the pathogenesis of co-infection with influenza virus and bacteria.