bluuebunny/crossref_metadata_2025_split huggingface dataset:
In vitro activation of rGM‐CSF derived bone marrow macrophages by cisplatin and lipopolysaccharide
Authors: SODHI AJIT , SURESH ALAPARTHY , SINGH SUKH MAHENDRA 
Published: July 2007

SummaryTreatment of fresh non‐adherent bone marrow cells (NABMC) with cisplatin or lipopolysaccharide (LPS) did not render them tumoricidal. NABMC incubated in medium alone or medium containing recombinant granulocyte macrophage colony stimulating factor (rGM‐CSF) for 4 days matured to macrophages that were positive for non‐specific esterase staining. Bone marrow‐derived macrophages cultured with medium alone did not respond to cisplatin or LPS by the induction of tumoricidal activity, whereas rGM‐CSF derived bone macrophages showed significantly enhanced cytotoxicity after treatment with cisplatin or LPS. Culturing of NABMC with rGM‐CSF enhanced cell survival compared to the cells incubated in medium alone. These results suggest that bone marrow cells not only mature in rGM‐CSF, but are also primed by rGM‐CSF for induction of tumoricidal activity.
CD‐13 (‘gp150’; aminopeptidase‐N): Co‐expression on endothelial and haemopoietic cells with conservation of functional activity
Authors: FAVALORO EMMANUEL J. 
Published: July 2007

SummaryThis report details experimental results which show the presence of enzymic aminopeptidase‐N‐like activity on endothelial cells, concomitant with cell surface expression previously detected by both ELISA and indirect immunofluorescence. This activity, detected using selected chromogenic substrates in functional assays, is shown to be due (at least in part) to a molecule previously termed'gp 150’and recognized by MoAb belonging to CD‐13, since such antibodies can he shown to inhibit this activity. Activity, as detected on endothelial cells, is similar to that observed on various haemopoietic cells. These assays not only provide a functional basis to cell Surface gp 150 (CD‐13) co‐expression on haemopoietic and endothelial cells but have also been used to help define structural epitopes present on aminopeptidase‐N/gpl 50, previously analysed using radiolabelled antibodies in competitive binding assays. Appraisal of these new data suggests that the number of distinct antibody binding sites on this molecule is greater than that previously demonstrated. This study is therefore an important first step in investigating the potential involvement of this selective peptidase molecule in the control of haemopoietic cell growth and differentiation and in haemostatic mechanisms.
Modulation of the immune response by tachykinins
Authors: EGLEZOS ANTHONY , ANDREWS PAUL V. , BOYD RICHARD L. , HELME ROBERT D. 
Published: July 2007

SummaryNeuro‐immunology is becoming an increasingly important discipline of immunology. This review has examined the immunomodulatory function of one group of neuropeptides, the TK, particularly SP and NKA. These peptides are localized in primary afferent nerves which have been shown to innervate several immune organs. In addition, binding sites for the TK have been demonstrated in thymus, spleen and lymph node. Several immune cell types also express neurokinin receptors including human circulating lymphocytes with binding to the Th/i class predominating, murine T and B cells, a human T lymphoblastoid cell line, human monocytes, rabbit polymorphonuclear leucocytes and guinea‐pig macrophages. The apposition of nerves with immune cells and receptors for neuropeptides thus produces an environment for interaction between the nervous and immune systems.Studies in vitro and, more recently, in vivo have examined how the TK regulate immune cell responses. The TK stimulate proliferation of T cells, enhance mitogen‐induced release of cytokines including IFN‐γ, TNF‐α, IL‐1 and IL‐6 from mononuclear cells and macrophages, enhance immunoglobulin secretion and affect cellular chemotaxis and phagocytosis. Studies in vivo have shown a role for TK in lymphocyte recirculation of sheep lymph nodes, reversal of stress‐induced thymic involution and Ig production in both rat and mouse. Many of these effects appear to be mediated via NK‐2 type receptors.To date, most of the work has involved studies in vitro, but the results from these are now being validated by studies in vivo where both the immune system and neuropeptides are able to interact at many anatomical sites. The complexities of the immune and the nervous systems mean that only a small number of potential interactions has been examined. Future studies can be expected to amplify these observations, especially with respect to the understanding of inflammatory and immune diseases in humans.
Serum factors affecting the specificity of anticardiolipin antibodies
Authors: LAYTON GUY T. , JOHNSTON SHANE C. , BERTWISTLE NEVILLE G. 
Published: July 2007

SummaryThe effects were investigated of two pretreatments of human serum and plasma test samples on their subsequent reactivity in the anticardiolipin antibody enzyme‐linked immunosorbent assay (ACA‐ELISA).The first treatment involved heat inactivation of test samples at 56°C for 30 min, a process sometimes used to inactivate samples from suspected human immunodeficiency virus positive individuals. Such treatment significantly increased the IgG ACA unit/mL values of normal sera, but when this effect was examined further, it was found that the increase in binding occurred on both cardiolipin‐coated and uncoated wells and was therefore non‐specific. Heat inactivation of sera prior to ACA testing should therefore be avoided.The second treatment involved diluting immunoglobulin (ig)G and IgM ACA‐positive sera in normal human serum (NHS) or newborn calf serum (NCS); sera diluted in NHS showed a significant increase in titre, particularly IgM ACA‐positive sera. This phenomenon was found to be due to a serum cardiolipin‐binding cofactor which enhances antibody recognition. The cofactor is heat stable and is present in normal sera (male and female) and also in IgG ACA‐positive sera. The binding of a human IgM monoclonal antibody to cardiolipin was not affected by the cofactor. The cardiolipin/cofactor complex may represent the optimal autoantigen/autoimmunogen and are‐appraisal, therefore, of the clinical relevance of antibodies to cardiolipin and other negatively charged molecules is warranted.
Effect of high ligand concentration on West Nile virus‐specific T cell proliferation
Authors: KULKARNI A. B. , MULLBACHER A. , BLANDEN R. V. 
Published: July 2007

SummaryIn this paper the phenomenon of suppression of proliferation in vitro of 14 day primed, West Nile Virus (WNV)‐specific, murine CD4+ T cells by large numbers of antigen‐presenting macrophages and B cells has been investigated. Suppression was apparently not mediated by prostaglandins, as the use of indomethacin in cultures at four times the usual concentration did not reverse suppression.Experiments were designed to evaluate the contribution of major histocompatibility complex (MHC) Class II and nominal WNV antigens in causing suppression of T cell proliferation. Listeria‐ or thioglycollate‐induced macrophages from CBA/H (H‐2k) mice, when treated with heat‐killed Listeria in vitro for 1 h to maintain or increase, respectively, MHC Class II levels before the addition of alloreactive Iak‐specific T cells caused inverse dose‐responses; the highest T cell proliferation occurred at a stimulator to responder (S:R) ratio of 0.25 and profound suppression at a S: R ratio of 1 or 2. In contrast, untreated thioglycollate‐induced macrophages, which express low MHC Class II levels, gave a direct dose‐response with increasing T cell proliferation as antigen‐presenting cell (APC) numbers increased.Addition of anti‐Ia antibodies (or their Fab fragments) to cultures caused a significant reversal of suppresion of anti‐WNV T cells imposed by high numbers of Listeria‐induced macrophages or 14 day WNV‐primed B cell APC. Suppression was also reversed by reducing the concentration of WNV antigen. These observations support the notion that the suppression of T cell proliferation observed at high S: R ratios was due to high concentrations of ligand (WNV‐derived peptide complexed with Class II MHC) on APC.
The effects of a leukaemia‐controlling dose of acivicin on murine splenic lymphocytes in vitro and in vivo
Authors: GRIFFITHS M. , KEAST D. 
Published: July 2007

SummaryThe development of successful chemotherapy for cancers, including leukaemia, is based on the exploitation of significant toxic differentials of the agents, between the cancer cells and their normal countilerparts. A concentration of 0.1 μmol/L of the amino acid analogue acivicin (L‐(α S.5S)‐α‐amino‐.Vchloro‐4,5‐dihydro‐5‐isoxazoleacetie acid) was sufficient to inhibit [3H]‐DNA synthesis in mitogen stimulated murine splenic lymphocytes and WEHI 7.1 murine loukaemic cells in vitro. at glutamine concentrations up to 0.5 μmol/L. However, al concentrations of glutamine of 1.0 μmol/Land above, more actvicin was required to inhibit WEHI 7.1 cells than to inhibit the splenic lymphovytes. At 1.0 mmol/L glutamine 18 h of exposure to an optimal inhibitory concentration of actvicin (0.5 μmol/L) in vitro was sufficient to inhibit [3H]‐DNA synthesis in the mitogen stimulated lymphocytes. whereas 24 h of exposure to an optimal inhibitory aciviein eoneeniration of 2.0 μmol/L was required for inhibition of [3H]‐DNA synthesis in the WEHI 7.1 leukaemic cells. When an actvicin inoeuhition regime that was sufficient to eontrol the growth of intraperitoneally (i.p. implanted WEHI 7.1 leukaemic cells was administered to Balb/c mice, the primary immune response was significantly inhibited loan anligen given either during orafler the actvicin treatment. These results indicale that lymphocytes replicating in vivo a specific primary immune response eould be as sensitive to actviein as leukaemic cells.
Interleukin‐2 activates the γ‐interferon gene in newborn mice
Authors: LIPOLDOVÁ MARIE , HOLÁŇ VLADIMÍR 
Published: July 2007

SummarySpleen cells from newborn mice are immunologically nonreactive and do not respond by proliferation upon stimulation with the T cell mitogen concanavalin‐A (Con‐A) or with recombinant interleukin‐2 (IL‐2). We have found that, in spite of the observed non‐reactivity in the proliferative tests, cells from newborn mice were able to synthesize a significant level of mRNA for γ‐interferon (γ‐IFN) after stimulation with IL‐2, but did not synthesize γIFN upon stimulation with Con‐A. Since γ‐IFN is of prime importance for antiviral and fungicidal activities and had complex regulatory functions for the cells of the immune system, we suggest that it could play an important role in the survival of newborns.
Down‐regulation of E1a expression by E3 gene products in group C adenoviruses
Authors: ZHANG XIAOLIU , MÜLLBACHER ARNO , BRAITHWAITE ANTONY W. 
Published: July 2007

SummaryMutant group C adenoviruses defective in expression of the E3 transcription unit were found to overexpress E1a proteins relative to wild‐type adenoviruses. This result suggests that one or more proteins encoded in the E3 region (present in wild‐type viruses) down‐regulate E1a expression. This interpretation was confirmed by transfection experiments in which a plasmid expressing the E3 region reduced expression of E1a in 293 cells. Experiments to examine the molecular basis of this down‐regulation of E1a suggest that E3 protein products interfere with the translation of viral mRNA molecules.
Expression of the high responder/non‐responder human FcγRII. Analysis by PCR and transfection into FcR COS cells
Authors: TATE BRUCE J. , WITORT EWA , McKENZIE IAN F. C. , HOGARTH P. M. 
Published: July 2007

SummaryDistinct differences in the capacity of monocyte FcγRII of different individuals to bin or not bind mouse IgG1 defines a polymorphism of FcγRIIa and has previously been defined as the high responder (HR) or low responder (LR) polymorphism of FcγRII. The precise definition of the molecular basis of the human HR/LR polymorphism of FcγRIIa from the peripheral blood mononuclear cells of normal individuals has been determined by anti‐CD3 induction of T cell proliferation, the polymerase chain reaction (PCR), nucleotide sequencing, transfection and IgG binding. Amplification of first strand cDNA from mRNA isolated from mononuclear cells was performed by PCR using primers specific for the sequences encoding the leader and cytoplasm sequences of FcγRIIa, which is normally expressed in monocytes. Sequencing of the PCR products and transfection of these to FcγR cells indicated that in FcγRIIa of HR or LR individuals; (i) three nucleotide substitutions (CA to TG and G to A) resulted in the change of glutamine to tryptophan at position 27 (first extracellular domain) and arginine to histidine at position 131 (second extracellular domain); (ii) expression of cDNA encoding the various combinations of these indicated that arginine at position 131 was essential for IgG1 binding whereas the amino acid changes at position 27 had no effect; and (iii) IgGf at high concentration bound to all allomorphic forms of FcγRIIa. These results indicate that position 131 in the second extracellular domain of FcγRIIa is intimately involved in immunoglobulin binding. Furthermore, the apparent inability of IgG1 to bind to FcγRIIa of non‐responder individuals is not absolute in that immune complexes sensitized with a high concentration of MIgG1 will bind to non‐responder‐type FcγRIIa.
Frequency of D8/17 B lymphocyte alloantigen in North Indian patients with rheumatic heart disease
Authors: GANGULY N. K. , ANAND I. S. , KOICHA M. , JINDAL S. , WAHI P. L. 
Published: July 2007

SummaryNinety patients with rheumatic heart disease and 50 age‐ and sex‐matched healthy human volunteers representing a North Indian population were typed for the B cell alloantigen D8/17 using a monoclonal antibody and a single step immunofluorescence technique. This alloantigen was expressed in 66.44% patients with RHD as compared with 14% of the normal population. A high relative risk (RR = 11.13) indicated a strong association of D8/17 B cell alloantigen with rheumatic heart disease. Increase in the frequency of the marker was observed with increasing age up to the fifth decade (40–49 years) in these patients. However, the frequency of this alloantigen, in the present study, in North Indian patients with rheumatic heart disease is lower than that reported in the American population.
Evaluation of thrombus detection in a rabbit model using a technetium‐99M‐labelled anti‐fibrin monoclonal antibody
Authors: LEE F‐T. , MILNER L. J. , BONIFACE G. R. , BAUTOVICH G. J. , WEEDON A. R. J. , BUNDESEN P. G. , RYLATT D. B. , WALKER K. Z. 
Published: July 2007

SummaryTechnetium‐99 m (99mTc)‐labelled conjugates of an anti‐fibrin monoclonal antibody, DD‐3B6/22, have been assessed for their detection of vascular thrombi in a rabbit model. DD‐3B6/22 binds to a D‐dimer epitope present on cross‐linked fibrin but absent from the fibrin monomer or fibrinogen. Injection of a 99mTc‐label led Fab′ fragment of DD‐3H6/22 allowed delineation of model thrombi as early as 30 min postinjection (p.i.) with optimal localization at 4–5 h. Thrombus label uptake at 4 h p.i. was 0.304 ± 0.106% injected dose/g (% ID/g) compared with 0.022 ± 0.001% ID/g after the injection of a control Fab′ fragment. These results suggest that the 99mTc‐labelled Fab′ fragment of DD‐3B6/22 has excellent potential for scintigraphic detection of vascular thrombi in humans.
Increased release of interleukin‐1 and tumour necrosis factor by interleukin‐2‐induced lymphokine‐activated killer cells in the presence of cisplatin and FK‐565
Authors: BASU SUNANDA , SODHI AJIT 
Published: July 2007

SummaryThe supernatants of peripheral blood lymphocytes cultured in interleukin‐2 (IL‐2) for 4 days contained tumour necrosis factor (TNF) and interleukin‐1 (IL‐1). Addition of cisplatin (CP) or FK‐565 to these cultures increased the level of both of these cytokines in culture supernatants. Furthermore, when the LAK cells induced by culture with IL‐2 in the presence or absence of CP/FK‐565 were co‐cultured with tumour cells, the production of these cytokines was significantly enhanced. The level of enhancement depended on the ratio of LAK cells to tumour cells used and the length of coincubation of the two cell types. Culture supernatants of LAK cells and LAK cells stimulated by tumour cells were also cytotoxic to MCF‐7 and U937 cells in 72 h cytotoxic assay, and antibodies specific for TNF and IL‐1 inhibited the supernatant‐mediated cytotoxicity. These results suggest that, in addition to the up‐regulation of IL‐2‐induced LAK activity, treatment of PBL with CP/FK‐565 leads to enhanced production of various cytokines with potential antitumour and immunoregulatory activity.
T cell receptor α‐chain polymorphic allele frequencies in Caucasians and Polynesians
Authors: GEURSEN A. , COUPER A. , ABBOTT W. G. H. , CAIRNS L. M. 
Published: July 2007

SummaryRestriction length polymorphisms in the variable and constant regions of the T cell receptor α‐chain were examined in 42 Caucasians, 29 Maoris and 27 Pacific Islanders. Southern blots of Tag I digested DNA were hybridized with the T cell receptor α‐chain probe pY14. Our results confirm that a 1.4 kb T cell receptor α chain‐Tag 1 band is allelic to a 0.5 kb band. A significant difference in the frequency of the 1.4 and 0.5 kb alleles of the variable region of the α‐chain was detected in Caucasians when compared with Maoris or Pacific Islanders (P < 0.0001). No differences in the frequency of the 2.0 and 7.0 kb alleles of the constant region gene were detected between any of the racial groups. These data may be relevant to ethnic differences in susceptibility to immune disorders.
Parasite‐induced changes to localized erythrocyte membrane deformability in Plasmodium falciparum cultures
Authors: NAUMANN KELLIE M. , JONES GRAHAM L. , SAUL ALLAN , SMITH ROSS 
Published: July 2007

SummaryThe effect of intra‐erythrocytic development of the Plasmodium falciparum parasite on local deformability of human erythrocyte membranes was studied by aspiration of cells into 0.56 μm diameter pores in polycarbonate filters and examination, after fixing, with a scanning electron microscope. As the aspiration pressure increased, the erythrocyte membrane was extruded into the filter pores. The pressure dependence of the protrusion length and the minimum pressure required to produce any deformation provided measures of the membrane shear and the bending moduli, respectively. At the trophozoite and, to a greater extent, schizont stage of development, host cell membrane deformability was significantly decreased. There was no appreciable difference between uninfected and ring‐infected erythrocytes.
Limiting dilution analysis in leprosy
Authors: MULLINS RAYMOND J. , ROCHE PAUL , ADAMS ELIZABETH , JONES PHILLIP , CHEN SHARON , THEUVENET WIM , BASTEN ANTONY 
Published: July 2007

SummaryPeripheral blood mononuclear cells (PBM) obtained from leprosy patients and healthy controls were cultured with Mycobacterium leprae and the control antigens, BCG and SKSD. Parallel cultures were supplemented with additional interleukin‐2 (IL‐2). On the basis of the level of response to M. leprae, leprosy patients could be divided into low, intermediate and high responders. The addition of IL‐2 resulted in enhanced proliferation to antigen only by cells from intermediate responders. This effect was neither antigen specific nor was it confined to cells from leprosy patients. When limiting dilution analyses were performed on cells from 26 patients across the leprosy spectrum, no M. leprae‐reactive lymphocytes were detected in cells from subjects with lepromatous disease. The precursor frequency for cultures containing M. leprae plus IL‐2 was no greater than that of cultures containing IL‐2 alone, thereby excluding the possibility of clonal anergy reversible with IL‐2. This was observed in both untreated patients and those on long‐term treatment, which made sequestration of antigen‐reactive cells within leprosy lesions an unlikely explanation. On the other hand, M. leprae‐reactive lymphocytes were detected in patients with tuberculoid and borderline tuberculoid disease and in two subjects with borderline lepromatous leprosy in type I reversal reaction. IL‐2 reactive cells were detected in all patients regardless of clinical classification. Three 'suppressor’curves were obtained but were not confined to cells from lepromatous patients. Taken together, these findings suggest that the non‐responsiveness to M. leprae characteristic of the great majority of multibacillary patients is due to an absence of antigen‐sensitive T cells.
Antibodies to 65 kDa and 70 kDa heat shock proteins in rheumatoid arthritis and systemic lupus erythematosus
Authors: PANCHAPAKESAN JAI , DAGLIS MALAMA , GATENBY PAUL 
Published: July 2007

SummaryTo test the potential role of autoimmunity to the highly conserved heat shock proteins (HSP) in immune arthritides, the sera from 99 patients with rheumatoid arthritis (RA), 48 patients with systemic lupus erythematosus (SLE) and 65 normal controls were examined by ELISA for IgG and IgM antibodies to the 65 kDa and 70 kDa heat shock proteins from Mycobacterium bovis (Bacille Calmette‐Guerin; BCG). In RA sera there are significant numbers of individuals with increased IgM anti‐65 kDa and anti‐BCG reactivity as well as IgG anti‐70 kDa when compared with controls. In SLE both IgM and IgG anti‐BCG, together with IgM anti‐65 kDa, differed significantly from controls. The results were compared with previous reports in similar groups of patients, and it is clear that no consistent pattern of reactivity emerges. While further work may be justified looking carefully at the disease duration and other subsets of both RA and SLE, it is difficult at this stage to conclude that antibodies to autologous HSP that cross‐react with mycobacterial HSP play a major role in disease pathogenesis.
Local immunity in the male reproductive tract
Authors: CLIFTON VICKI L. , HUSBAND ALAN J. , KAY DAVID J. 
Published: July 2007

SummaryIn previous studies we have demonstrated that the male urinary tract forms part of the common mucosal immune system, and that the gut contributes to local defences at this site.1 The question arises as to the extent to which the reproductive tract also forms part of the common mucosal immune system. Rats were immunized by a variety of routes designed to stimulate a local response in the intestine and/or the reproductive tract. Rats immunized only by the intratesticular (i.t.) route yielded no antibody‐containing (ACC) response in any of the tissues examined. Intestinal immunization using intraperitoneal priming followed by intraduodenal challenge (i.p./i.d.) yielded a substantial IgA‐specific ACC response in the jejunum, but no ACC were detectable in any of the reproductive tract tissues. However, when intestinal and testicular immunizations were combined, large numbers of IgA‐specific antibodies were detected in all tissues examined. Chronic drainage of the thoracic lymphatic duct throughout the post‐challenge period abrogated the ACC response in all tissues of the reproductive tract, indicating that the ACC appearing at these sites after immunization were of gut origin. The IgA‐specific anti‐OVA antibody detectable in serum, saliva and testis homogenate reflected the ACC counts in histological sections. The studies reported here confirm that the male reproductive tract does form part of a common mucosal immune system and that gut‐associated lymphoid tissues may contribute cellular precursors for ACC, particularly those of IgA specificity, appearing in the tract after local challenge. The implications of these findings to infectious disease involving the urogenital tract are obvious and investigation of oral vaccines to control sexually transmitted disease as well as acquired urinary tract infections deserves further attention. There are further implications, however, for the understanding and management of male infertility.