bluuebunny/crossref_metadata_2025_split huggingface dataset:
Spontaneous proliferation of memory (CD45RO+) and naive (CD45RO-) subsets of CD4 cells and CD8 cells in human T lymphotropic virus (HTLV) infection: distinctive patterns for HTLV-IversusHTLV-II
Authors: Prince H E , York J , Owen S M , Lal R B 
Published: July 2010

SUMMARYSpontaneous lymphocyte proliferation (SLP) in vitro is a characteristic feature of about 50% of individuals infected with HTLV-I or HTLV-II. Both CD4 cells and CD8 cells contribute to SLP in HTLV-I infection, whereas SLP in HTLV-II infection is usually restricted to CD8 cells. In this study, we asked if SLP was restricted to the memory (CD45RO+) cell subset of CD4 and CD8 cells in HTLV infection. Purified CD4 and CD8 cells were separated into CD45RO+ and CD45RO- populations by a modified panning technique, and spontaneous proliferation (SP) of the cell subsets was assessed. For all five HTLV-I-infected persons whose mononuclear cell cultures were SLP+, only CD45RO+ cells, but not CD45RO- cells, within CD4 and CD8 subsets showed SP. In contrast, five of six SLP+ HTLV-II+ individuals showed SP in both the CD45RO+ and the CD45RO- subsets of CD4 cells, and 10 of 12 SLP+ HTLV-II+ individuals showed SP of both the CD45RO+ and CD45RO- subsets of CD8 cells. Polymerase chain reaction studies showed that proviral genome was generally present in both CD45RO+ and CD45RO- subsets of CD4 and CD8 cells, regardless of HTLV type and SP activity. These findings show that SP of both CD4 and CD8 cells in HTLV-I infection is usually restricted to CD45RO+ memory cells, whereas in HTLV-II infection, both CD45RO+ memory and CD45RO- naive subsets of CD4 and CD8 cells may exhibit SP. It thus appears that HTLV-I infection and HTLV-II infection exhibit distinctive dysregulatory effects on memory and naive T cell subpopulations.
The restricted IgG1 antibody response to maedi visna virus is seen following infection but not following immunization with recombinantgagprotein
Authors: Bird P , Reyburn H T , Blacklaws B A , Allen D , Nettleton P , Yirrell D L , Watt N , Sargan D , Mcconnell I 
Published: July 2010

SUMMARYMaedi-visna (MVV) is a retrovirus of the subfamily lentivirinae which includes HIV, simian immunodeficiency virus (SIV) and feline immunodeficiency virus (FIV), infection of its natural host, the sheep, does not cause overt immunodeficiency, but rather a chronic inflammatory disease. However, subtle immunological changes following infection have been reported including a sheep IgGi subclass-restricted MVV-neutralizing antibody. Here we demonstrate by Western blotting that there is no IgG2 serum antibody response to any MVV antigen after MVV infection, in contrast to infection with the parapox virus Orf, when serum IgG2 anti-Orf antibody is readily detected. By ELISA, the IgGi antibody titres to Orf are higher than to MVV, but the minimum MVV serum antibody IgG1/IgG2 ratio is significantly raised compared with that for Orf virus antibody in the same sheep, indicating that the IgG2 defect in MVV infection cannot be accounted for by differences in the sensitivity of the Orf and MVV ELISA. Serum IgG2 anti-MVV gag p. 25 can be detected in both normal and MVV-infected sheep following immunization with purified recombinant MVV gag p 25 protein in Freund's complete adjuvant. The failure to make an IgG2 MVV-specific antibody indicates that immunological dysfunction can arise with macrophage tropic lentiviruses, and it may aid viral persistence.
Lupus-derived autoantibodies with dual autoactivity: anti-DNA and anti-Fc. II. Fine specificity of anti-self autoreactivity
Authors: Rumbley C A , Voss E W 
Published: July 2010

SUMMARYThe anti-immunoglobulin reactivity of two monoclonal, dual specific, autoantibodies, BV 17–45 and BV 04-01 was examined. The current study further defined the anti-immunoglobulin autoreactivity of these MoAbs to be Fc-specific. Both BV 17–45 and BV 04-01 bound their own Fc domains in addition to Fc regions of other MoAbs of similar isotype with varying levels of activity. The different anti-Fc reactivity patterns of BV 17–45 and BV 04-01 suggested that these MoAbs recognized distinct epitopes. Neither BV 17–45 nor BV 04-01 bound Fab fragments or single-chain antibody derivatives, which confirmed that the anti-immunoglobulin reactivity of these autoantibodies was Fc-specific. In addition, abrogation of anti-Fc reactivity was observed when affinity-labelled MoAbs were used as coating antigens in solid-phase ELISAs. These results implied that active-site ligand binding induced cotiformational changes which altered the Fc epitope(s) recognized by BV 17–45 and BV 04-01.
Prevention of adoptive transfer of murine Sjögren's syndrome into severe combined immunodeficient (SCID) mice by antibodies against intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1)
Authors: Hayashi Y , Haneji N , Yanagi K , Higashiyama H , Yagita H , Hamano H 
Published: July 2010

SUMMARYWe have analysed the role of ICAM-1 and LFA-1 during development of autoimmune sialadenitis in MRL/1pr mice by direct analysis of RNA obtained from the salivary gland tissues, and the therapeutic effects with antibody administration on adoptive transfer system into SCID mice. The expression of cell adhesion molecules was assessed by using reverse transcriptase polymerase chain reaction (RT-PCR) and Southern blot analysis, and immunohistochemical analysis. Up-regulated expression of ICAM-1 mRNA was observed before the onset of inflammatory lesions in the salivary glands at 1 month and 2 months old, and thereafter LFA-1 mRNA was expressed within the typical inflammatory lesions, resembling human Sjögren's syndrome in MRL/1pr mice. Immunohistochemically, ICAM-1 was localized exclusively in the endothelial cells of varying sized blood vessels before the onset of disease, and LFA-1 expressing inflammatory ceils were found within these lesions. When the therapeutic effects in vivo were examined, antibodies to ICAM-1 in combination with anti-LFA-1 prevented adoptive transfer of Sjögren's syndrome in MRL/1pr mice into SCID mice, while no significant effect was found when treated with either antibody. These findings ìndìcate that in Sjögren's syndrome-like autoimmune lesions in MRL/1pr mice the ICAM-1/LFA-1 pathway may play a crucial role in the initiation and subsequent progression of T cell-mediated autoimmunity in the salivary and lacrimal glands of MRL/1pr mice.
Measurement of IL-4 in tears of patients with seasonal allergic conjunctivitis and vernal keratoconjunctivitis
Authors: Fujishima H , Takeuchi T , Shinozaki N , Saito I , Tsubota K 
Published: July 2010

SUMMARYTo elucidate the mechanism of ocular surface allergic disease, we focused on IL-4, which is one of the key factors in regulating IgE production, and thus determined the concentration of IL-4 in tears, IL-4 concentration was determined in the tears of 15 patients with seasonal allergic conjunctivitis, 15 vernal keratoconjunctivitis (VKC), 10 giant papillary conjunctivitis (GPC), 10 patients with non-allergic conjunctivitis and post-cataract surgical conjunctivitis as intermediate conjunctivitis, and 10 normal subjects using a highly sensitive sandwich ELISA. The mean level of IL-4 in normal controls was low, and seasonal allergic conjunctivitis, VKC and GPC showed a significant elevation (P &lt; 0.05), respectively. IL-4 of VKC and GPC were also significantly higher than allergic conjunctivitis, and non-allergic conjunctivitis and post-cataract surgical conjunctivitis were not higher than normal. These results raise the possibility that the increased level of IL-4 in tears could play a role in allergic disease and its severity in patients.
A possible role for lysozyme in determining acute exacerbation in chronic bronchitis
Authors: Taylor D C , Cripps A W , Clancy R L 
Published: July 2010

SUMMARY
The aggregation of non-serotypable Haemophilus influenzae (NTHI) by whole saliva from patients with chronic obstructive lung disease (COLD) was investigated. Significant differences were observed between salivary aggregating activity of a control and COLD population (P &lt; 0·001). Saliva from patients less prone to acute exacerbations had a greater capacity to aggregate bacteria compared with saliva from patients with a predilection to infection. The mechanism of saliva-mediated aggregation of NTHI was investigated and shown to be related to lysozyme content. Lysozyme activity in saliva was measured by the turbidimetric technique and results showed that patients with chronic bronchitis had increased levels of salivary lysozyme, with a subpopulation within the non-infection-prone group having greater amounts. A significant difference was observed in salivary lysozyme between controls and non-infection-prone (P &lt; 0·005) and infection-prone (P &lt; 0·05) patients, respectively: the non-infection-prone patients having significantly (P &lt; 0·005) more than the infection-prone patients. There was significant correlation (r= 0·742, P &lt; 0·001) between salivary aggregation of NTHI and lysozyme activity. Chromatographically purified human lysozyme had a similar aggregation profile to that of saliva. There was no difference in serum and saliva lactoferrin concentrations between groups, but there was a significant increase (P &lt; 0·05) in serum lysozyme concentration in the non-infection-prone group. This study suggests that the level of salivary lysozyme derived from macrophages may play an important role in determining resistance or susceptibility to acute bronchitis.
Functional platelet-derived growth factor-beta (PDGF-β) receptor expressed on early B-lineage precursor cells
Authors: Trink B , Wang G , Shahar M , Meydan N , Roifman C M 
Published: July 2010

SUMMARYGrowth and maturation of B lymphocytes from stem cells require a series of complex processes that are dependent at least in part on growth factors. Uncontrolled expression of receptors from these early growth factors may contribute to a leukaemogenesis of such early B cell progenitors. We show here that early pre-pre-B cells, but not mature B cells, express the PDGF receptor-beta (PDGFR-β). These receptors contain a protein tyrosine kinase domain which is activated upon ligation with PDGF in pre-pre-B cells. Further, pre-pre-B leukaemia cells seem to express more PDGFR-β compared with their normal counterparts, suggesting a role for these receptors in growth promotion of leukaemia cells.
Immunotherapy with monoclonal antibodies directed against the immunosuppressive domain of p15E inhibits tumour growth
Authors: Lang M S , Hovenkamp E , Savelkoul H F J , Knegt P , Van Ewijk W 
Published: July 2010

SUMMARY
Immunosuppressive retrovirus-related proteins, like p15E, are involved in tumour-associated immunosuppression. In the present study we investigated whether such proteins could be used as targets in tumour immunotherapy using MoAbs. Immunotherapy was performed in mice inoculated with the Rauscher virus-transformed myeloid cell line RMB-1. RMB-1 cells express retroviral antigens at their cell surface. In order to obtain constant scrum titres of MoAbs over a prolonged period of time during therapy, anti-pl 5E antibody-producing hybridoma ceils were encapsulated in alginate and injected intraperitoneally in tumour-bearing mice. Using this technique, serum antibody titres of 50–100μg/ml were obtained, which remained constant over a period of at least 3 weeks. Therapy experiments were performed using anti-p15E antibodies 1F8, which recognizes both cell surface-associated as well as circulating pi 5E. and ER-1S5, which did not react with surface-bound p15E beyond background, but which neutralizes circulating p15E. Inoculation of alginates containing anti-p15E hybridoma cell lines in RMB-1 tumour-bearing mice showed inhibition of tumour cell growth. In survival experiments, 19F8 cured eight of 23 tumour-bearing mice. The p 15E neutralizing antibody ER-IS5 caused a significant longer survival, but therapy with this MoAb alone was not sufficient to cure the animals of the RMB-1 tumour.
Effect of adjuvants on immunization with dengue virus-induced cytotoxic factor
Authors: Mukerjee R , Chaturvedi U C 
Published: July 2010

SUMMARY
Specific active immunization with dengue type 2 virus (DV)-induced cytokine. cytotoxic factor (CF), prevents CF-mediated pathology in mice. The present study was undertaken to determine the optimum dose of CF and the effect of different adjuvants on the immune response as assessed by the study of anti-CF antibody titre by ELISA and protection against increase in capillary permeability to challenging dose of 3 μg CF. The maximum protection of 94 ± 4% against increase in capillary permeability was observed at week 4 after immunization with 5 μg dose of CF mixed with Freund's incomplete adjuvant (FIA), which gradually decreased to 21 ± 10% on week 24. With a dose of 10 μg the protection obtained was 79±5%, but persisted for a longer time at a higher level. The response was poor with 1 μg dose of CF. The mean anti-CF antibody titres gradually decreased after reaching the peak at week 4 after immunization. Mice immunized with different adjuvants emulsified with 5μg CF were challenged at different intervals with 3μg CF. Maximum protection observed with CF + tetanus toxoid (TT) and 84/246 was about 93 ± 2% and 97 ± 2% while that with alhydrogel was 33 ± 12% and with bacille Calmette-Guérin(BCG) was 67±4%. At week 24 after immunization, however, the best response was obtained with 10μg of adjuvant 84/246. Intracerebral challenge with 10 or 100 LD50 dose of dengue type 2 virus showed significantly prolonged mean survival time and delayed onset of signs of sickness in immunized mice compared with normal mice. The maximum survival time was with adjuvant 84/246 even at week 24, The findings thus show that the optimum dose of CF is 5 μg and the adjuvant of choice is 84/246.
Increased expression of proopiomelanocortin (POMC) mRNA in adrenal glands of mice undergoing graft-versus-host disease (GVHD); association with persistent elevated plasma corticosterone levels
Authors: You-Ten K E , ItiÉ A , Seemayer T A , Palfree R G , Lapp W S 
Published: July 2010

SUMMARYGVHD in animal models induces severe thymic atrophy as a result of prolonged secretion of high concentrations of adrenal glucocorticoids. In this study we investigated the mechanism responsible for the persistent stimulation of the adrenal glands to secrete glucocorticoids in mice undergoing GVHD. GVHD was induced across the major and multiple minor histocompatibility antigen difference in unirradiated C57B1/ 6x AFI hybrid mice by the intravenous injection of A strain parental lymphoid cells. Our results showed plasma corticosterone (CS) levels were elevated in association with high concentrations of corticotropin (ACTH) in both the GVHD and control syngeneic (SYN) groups on day 9. By days 16 and 24. plasma CS and ACTH in the SYN mice returned to basal levels. In contrast, plasma CS levels remained elevated in the GVHD animals on days 16 and 24 despite decreasing concentrations of plasma ACTH. Reverse transcription-polymerase chain reaction (RT-PCR) showed several-fold increase in POMC mRNA in the adrenal glands of GVHD mice compared with SYN animals. In addition, high mRNA levels for murine prohormone convertase 1, the enzyme that cleaves POMC into ACTH, were also detected in GVHD adrenals. Histological analysis of GVHD adrenals failed to show any sign of adrenalitis, and RT-PCR of GVHD adrenals also failed to detect mRNA for interferon-gamma (IFN-γ), a cytokine expressed by activated T and natural killer (NK) cells. However, mRNA for IL-12, a cytokine produced by activated macrophages, was increased in GVHD adrenals, suggesting that resident adrenal macrophages were activated during GVHD. Our findings suggest that persistent elevated levels of plasma glucocorticoids during GVHD could be mediated by intra-adrenal ACTH produced by resident adrenal macrophages activated as a consequence of GVHD.
Antigen processing and presentation by a murine myoblast cell line
Authors: Garlepp M J , Chen W , Tabarias H , Baines M , Brooks A , McCluskey J 
Published: July 2010

SUMMARYThe ability of non-professional antigen-presenting cells (APC) lo process and present antigen to the immune system has been the subject of debate in autoimmunity and tumour immunology. The role of muscle cells in the processing and presentation of antigen to T cells via class 1 and class II MHC pathways is of increasing interest. Muscle cells are the targets of autoimmune attack in the inflammatory muscle diseases, and direct intramuscular injection of antigen-expressing DNA constructs is under scrutiny as a means of vaccination. Furthermore, the immunological properties of muscle cells are of relevance in attempts to transfer my oblasts as replacement cells in dystrophic diseases or as depot cells for the secretion of certain molecules in deficiency states. Using class I and class II MHC transfectant clones of the C2CI2 my oblast cell line, my oblasts have been shown to be capable of presenting antigen to. and stimulating secretion of IL-2 by, T cell hybridomas via both of these pathways. The epitopes which are dominantly presented by professional APC after processing of native antigens were also presented by the myoblast cell line after processing of either ovaibumin (class I) or hen egg lysozyme (class 11). Further, antigen processing and presentation via the class II pathway were enhanced by pretreatment of the my oblasts with interferon-gamma (IFN-γ), Up-regulation of invariant chain expression by this treatment may have contributed to this enhanced presentation, but an effect of IFN-γ on the expression of other molecules such as H-2 DM may have also played a role. The demonstration of the antigen-presenting properties of these my oblasts is of relevance to all three areas mentioned above. In each situation my oblasts comprise a significant population within muscle. In the case of inflammatory muscle diseases the process of muscle degeneration and regeneration is on-going, while in the vaccination procedure some muscle damage occurs, and vaccination is more effective when muscle damage has preceded inoculation.
Exposure to hyperbaric oxygen induces tumour necrosis factor-alpha (TNF-α) secretion from rat macrophages
Authors: Lahat N , Bitterman H , Yaniv N , Kinarty A , Bitterman N 
Published: July 2010

SUMMARYWe investigated the secretion of TNF-α by monocytes and macrophages derived from the peripheral blood, spleen, and lungs after a single exposure to a therapeutic profile of hyperbaric oxygen (HBO). Rats were exposed for 90 min to either 100% oxygen at 0 28 MPa (2–8 atmospheres absolute) or air. Immediately after exposure, mononuclear cells were isolated from blood, spleen, and lungs and cultured for 18h. The secretion of TNF-α from the cultured monocytes/macrophages was determined with and without stimulation with lipopolysaccharide (LPS). Exposure to hyperbaric oxygen induced a significant increase in the spontaneous ex vivo secretion of TNF-α (without LPS) by mononuclear cells from the blood, spleen, and lung (P &lt; 0 05 from air controls). Stimulation with LPS after exposure to HBO induced a significant increase in TNF-α secretion by lung and spleen macrophages compared with air controls (P&lt;005). However, absolute TNF-α levels were not significantly higher than those achieved ‘spontaneously’ in macrophages exposed to HBO without LPS. Stimulation with LPS induced a marked increase in secretion of TNF-α from blood monocytes after exposure to air, but not after exposure to HBO. These results provide evidence in support of a role played by TNF-α in mediating HBO effects on different tissues and their immune responses.
The immunosuppressive drug thalidomide induces T helper cell type 2 (Th2) and concomitantly inhibits Th1 cytokine production in mitogen- and antigen-stimulated human peripheral blood mononuclear cell cultures
Authors: Mchugh S M , Rifkin I R , Deighton J , Wilson A B , Lachmann P J , Lockwood C M , Ewan P W 
Published: July 2010

SUMMARYThalidomide is an effective immunomodulatory drug in man, but its mechanism of action remains unclear. We hypothesized that, in addition to its reported inhibitory effects on production of monocyte-derived tumour necrosis factor-alpha (TNF-α), thalidomide might be effective at the level of Th immunoregulation. In a comparative study with the immunosuppressant cyclosporin A, we have demonstrated a potent and specific effect of thalidomide on cytokine production relating to the distinct Th1 and Th2 subsets. It induced and enhanced the production of IL-4 and IL-5 and, at the same dose (1000 ng/ml), significantly inhibited interferon-gamma (IFN-γ) production in phytohaemagglutinin (PHA)-stimulated human peripheral blood mononuclear cell (PBMC) cultures. Stimulation of PBMC with recall antigen (streptokinase:streptodornase (SKSD))at 144h in the absence of thalidomide resulted in a predominantly Th1 response, with the production of IFN-γ and IL-2. Thalidomide switched this response from a Th1 to a Th2 type. The effect was most pronounced at 1000 ng/ml thalidomide, where inhibition of IFN-γ and enhancement of IL-4 production was maximal. In unstimulated cultures thalidomide alone induced IL-4 production. Cyclosporin A, in contrast, inhibited both Th1 and Th2 cytokine production by PHA-stimulated PBMC. Time course data from thalidomide-treated cultures revealed that the augmented IL-4 production diminished as the culture time increased, whereas IFN-γ production was significantly increased. This response might be due to activation-induced apoptosis of Th2 cells or the induction of Th2 cell anergy, in the continued presence of stimulating agents, with the emergence of IFN-γ-secreting Th1 cells when Th2 antagonism declines. The effects of thalidomide and related compounds may enhance our understanding of the mechanisms of T helper cell selection, offer the possibility of controlled therapeutic switching between Th1 and Th2 responses, and may lead to a rational approach for the treatment of some T cell-mediated immunological disorders.
Secretion of immunoglobulins and plasma proteins from the colonic mucosa: anin vivostudy in man
Authors: Prigent-Delecourt L , Coffin B , Colombel J F , Dehennin J P , Vaerman J P , Rambaud J C 
Published: July 2010

SUMMARYThere are no available data on immunoglobulins and albumin outputs into the normal human colon. We thus measured the intracolonic secretion rates of IgA, IgG, IgM, secretory component (SC) and plasma proteins (albumin (Alb), orosomucoid (Oro), transferrin (Transf) and α2-macroglobulin (α2-M)). Using a pancolonic perfusion technique in 10 healthy volunteers (six females, four males, mean age 24 years), concentrations and outputs of Alb, immunoglobulins, SC, Oro, Transf and α2-M were measured in the rectal effluents by immunoradiometric assay. Monomeric (m) and polymeric (p) IgA distribution was analysed by sucrose density ultra-centrifugation. The secretion of polymeric IgA (p-IgA) was 153 μg/min, i.e. 220 mg/day, exceeding that of other immunoglobulins (m-IgA 8·5 μg/min; IgG 33·5 μg/min; IgM 17μg/min) and of non-immunoglobulin proteins (Alb 104 μg/min; Oro 9 μg/min; Transf 7 μg/min; α2-M 4·5 μg/min), p-IgA was entirely linked to SC (secretory IgA) and 12% of SC was in free form. About 62% of total IgA was IgA2. For each protein, a relative coefficient of excretion (RCE) was calculated (colon to serum concentration ratio expressed relative to that of Alb). The p-IgA, IgM and m-IgA RCE were 277, 6 and 2·2 times higher than the values predicted from their molecular weight. RCE of non-immunoglobulin proteins also exceeded the values expected from a passive seepage from the vascular compartment. The intracolonic clearance of Alb extrapolated to 24 h was only 3·7 ml/day. These results show the high local production and/or the facilitated transport to the colonic lumen of p-IgA, and are in very good agreement with the distribution of plasma cells in the colonic mucosa.