bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cellular immunity in experimental Echinococcus multilocularis infection. II. Sequential and comparative phenotypic study of the periparasitic mononuclear cells in resistant and sensitive mice
Authors: BRESSON-HADNI S , LIANCE M , MEYER J P , HOUIN R , BRESSON J L , VUITTON D A 
Published: July 2010

SUMMARY
Cellular immune responses have been shown to be associated with differential evolutions of E. multilocularis infection in intermediate hosts. A relationship between course of delayed-type hypersensitivity (DTH) against parasitic antigens and receptivity of murine strains has been demonstrated recently. The aim of this study was to correlate resistance and sensitivity to E. multilocularis infection with the phenotypic patterns of cells within the periparasitic granuloma. Evolution of the ratios, macrophages/T lymphocyte and Lyl/Ly2 T lymphocytes, was associated with the receptivity of the strains. Persistence of numerous L3T44+T lymphocytes and low numbers of macrophages and Ly2+T lymphocytes were observed in the ‘resistant’ C57BL.10 mice. Comparison of the results with course of the DTH against E. multilocularis antigens showed that the particular phenotypic pattern observed in resistant mice was associated with a particular profile of DTH after infection. These results and similar observations in human alveolar echinococcosis suggest that cell composition of the periparasitic granuloma might be of crucial importance in controlling the spontaneous development of E. multilocularis larvae in the intermediate host.
Intra-articular immunization induces strong systemic immune response in humans
Authors: TROLLMO C , CARLSTEN H , TARKOWSKI A 
Published: July 2010

SUMMARYThere is no information available about immunological interactions between the synovial tissue compartment and systemic immunity in health and in disease. The aim of the present study was to evaluate effects of intra-articular immunization on the systemic immune responses in humans. Control subjects were immunized with the same dose of immunogen subcutaneously. Peripheral blood lymphocytes were analysed by spot-ELISA with respect to numbers of immunoglobulin-producing cells and antigen-specific antibody-secreting cells before and 1 week after immunization. Serum and salivary antibody levels were measured by an ELISA before and 14 days after the antigenic exposure. In addition, serum levels of interleukin-6 (IL-6) were analysed before and after immunization. The results indicate that the influenza virus antigen deposited in the joint space induces strong systemic antibody response of IgG, IgA and IgM classes. This response is significantly higher (P &lt; 0.05) than that of control subjects immunized subcutaneously. In contrast, no significant differences were detected between intra-articularly and subcutaneously immunized subjects with respect to mucosal immune responses. Increased serum levels of IL-6 were observed 1–2 weeks after the vaccination in both experimental groups. We conclude that human joints possess very efficient antigen-presenting properties enhancing systemic B cell reactivity.
Soluble HLA class I antigen secretion by normal lymphocytes: relationship with cell activation and effect of interferon-gamma
Authors: BRIEVA J A , VILLAR L M , LEORO G , ALVAREZ-CERMEÑO J C , ROLDÁN E , GONZALEZ-PORQUÉ P 
Published: July 2010

SUMMARYHLA class I antigens are thought to be integral membrane proteins. However, soluble forms of these molecules have been detected. Our laboratory has recently shown that the predominant form of these soluble proteins present in human serum, spleen tissue and culture supernatant of activated lymphocytes exhibits molecular weight and structure similar to classical HLA class I antigens, but lacks HLA A or B polymorphic determinants. In the present study, the secretion of such soluble proteins by lymphocytes has been further explored. Phytohaemagglutinin-stimulated normal lymphocytes secrete considerable quantities of soluble HLA (sHLA) class I proteins. This secretion seems to be a general property of lymphocytes, since activation of T as well as B cells by appropriate mitogens equally induce sHLA I secretion. Lymphocytes require RNA and protein synthesis, but not DNA synthesis, for the secretion to occur. Kinetic studies reveal that maximal sHLA I secretion precedes the peak of DNA synthesis by 24 h. In vitro stimulation with antigens or alloantigens also provokes sHLA I secretion. Moreover, this phenomenon has also been detected for in n'ro-aclivated lymphocytes, as enhanced spontaneous sHLA I secretion was observed in cultures of Low-density blastic B and T cells, and of blood lymphocytes obtained from normal subjects who had received a booster immunization 5 days earlier. Interferon-gamma (IFN-γ) increases the expression of membrane-bound class I antigens but does not induce any sHLA I secretion, suggesting that both molecules are under different regulatory mechanisms. Our results indicate that human lymphocytes, upon stimulation, actively secrete considerable amounts of a soluble form of these biologically relevant proteins.
Transforming growth factor-β1 inhibits activation of macrophage cell line RAW 264.7 for cell killing
Authors: HAAK-FRENDSCHO M , WYNN T A , CZUPRYNSKI C J , PAULNOCK D 
Published: July 2010

SUMMARYTransforming growth factor β-1 (TGF-β) is a multi-potent immunoregulatory peptide that has effects on numerous cell types. Here we report that human TGF-β inhibits the activation of the macrophagc cell line RAW 264.7 for killing of the L1210 tumour cell line. RAW 264.7 cells, like normal macrophages, require sequential interaction with priming and triggering stimuli for full activation of cytolytic activity. TGF-β inhibits this cytotoxicity in a dose-dependent manner at both the priming and the triggering stage. Addition of as little as 1 ng/ml TGF-β when added with either the priming signal, recombinant interferon-gamma (IFN-γ), or the triggering signal, bacterial lipopolysaccharide (LPS), completely abrogated tumouricidal activity. Incubation with TGF-β also inhibited the morphological changes normally observed in activated RAW 264.7 cells. However. TGF-β was unable to inhibit the cytotoxic activity of RAW 264.7 cells against the target cell line WEHI 164, which is sensitive to tumour necrosis factor. In contrast to the effects on cytotoxic activity, the cytostatic activity of activated RAW 264.7 cells was not inhibited by TGF-β at doses of up to 5 ng/ml. In addition, pretreatment of the LI210 target cells with TGF-β made them refractory to both the cytostatic and cytotoxic effects of RAW 264.7 cells. These data suggest that TGF-β may be an important mediator in the regulation of macrophage tumouricidal activity.
Dose-dependent increase in plasma interleukin-6 after recombinant tumour necrosis factor infusion in humans
Authors: SHERON N , LAU J N , HOFMANN J , WILLIAMS R , ALEXANDER G J M 
Published: July 2010

SummarySeveral studies have shown that the cytokine interleukin-6 (IL-6) is produced in response to tumour necrosis factor (TNF) in vitro. This study examines the in vivo relation between these two cytokines with assays of plasma IL-6 and TNF levels in subjects with chronic hepatitis B undergoing immunomoduiatory therapy with recombinant TNF(rTNF). Plasma IL-6 was detected from 20 min after rTNF infusion with levels peaking after 2–3 h and levels correlated with the dose of rTNF administered (r= 0.67,P=0.004). Peak levels of IL-6 (mean 295, range 266–297 ng/l) were lower than those seen in certain disease states despite the very high peak levels of rTNF (mean 11 750, range 5623-18 620 ng/l). These findings suggest that the very high levels of IL-6 found in certain disease states are not purely the result of circulating TNF. Other factors such as endotoxin or other cytokines may also play a role in determining levels of plasma IL-6.
Isotype-selective abrogation of established IgE responses
Authors: HayGlass K T , STEFURA W 
Published: July 2010

SummaryChemically modified allergens have been extensively studied in an attempt to develop materials of increased efficacy and improved safety for use in the immunotherapy of allergic disease. Most of the strategics that have been developed yield products that strongly inhibit de novo IgE responses but have only marginal impact on ongoing IgE responses. We report the virtual abrogation of pre-established murine anti-ovalbumin IgE responses using a glularaldehyde-polymerized ovalbumin preparation (OA-POL) of Mr 3.5 × 107. Secondary IgE responses are inhibited by 97–99% over a period of at least 8 months following three i.p. courses of OA-POL treatment. Administration of five additional ovalbumin [Al(OH)3] booster immunizations over tbis period fails to alter this unresponsive state. The inhibition of antigen-specific IgE responses is isotype specific.
An experimental influenza subunit vaccine (iscom): induction of protective immunity to challenge infection in mice after intranasal or subcutaneous administration
Authors: LÖVGREN K , KÅBERG H , MOREIN B 
Published: July 2010

SummaryAn experimental influenza virus (A/PR/8/34(H1N1)) vaccine was tested and evaluated in mice. The mice were inoculated once or twice intranasally or subcutancously with 1 or 10 μg of iscoins prior to challenge with high doses of live virus. It was demonstrated that two intranasal administrations were as efficient as two s.c. administrations, both routes inducing high levels of antibody and protection against challenge infection. With a one-dose regimen, the s.c. route induced a somewhat higher antibody response than the intranasal route; this might be explained by technical difficulties connected with an intranasal administration.
Tumour necrosis factor production in fulminant hepatic failure: relation to aetiology and superimposed microbial infection
Authors: DE LA MATA M , MEAGER A , ROLANDO N , DANIELS H M , NOURI-ARIA K T , GOKA A K J , EDDLESTON A L W F , ALEXANDER G J M , WILLIAMS R 
Published: July 2010

SummaryTumour necrosis factor-alpha (TNF-α), a cytokine derived from macrophages, is considered to bean important endogenous mediator of endotoxic shock. Patients with fulminant hepatic failure are particularly susceptible to infection and the development of multi-organ failure and similarities to endotoxic shock suggest a possible pathogenetic role for TNF in fulminant hepatic failure. In vitro TNF production was therefore investigated serially in 21 consecutive patients with fulminant hepatic failure and in 21 healthy controls. Spontaneous and lipopolysaccharide-stimulated TNF production were elevated in viral-induced fulminant hepatic failure, compared with healthy controls (P &lt; 0.05 and P &lt;0.01, respectively). By contrast, patients with paracetamol-induced fulminant hepatic failure had normal spontaneous and lipopolysaccharide-stimulated TNF production, while those who died had significantly reduced spontaneous TNF production compared with survivors (P &lt; 0.02); this difference was present throughout admission. In this group elevations in TNF production above baseline were associated with Gram-positive bacterial or fungal infection but not Gram-negative bacterial infection. There was no correlation between any of the clinical complications of fulminant hepatic failure and TNF production. These studies indicate that TNF is produced in response to microbial stimuli in fulminant hepatic failure, but do not support a direct role for TNF in the evolution of the clinical complications of fulminant hepatic failure.
Helicobacter pylori induces lymphocyte activation in peripheral blood cultures
Authors: KARTTUNEN R , ANDERSSON G , POIKONEN K , KOSUNEN T U , KARTTUNEN T , JUUTINEN K , NIEMELÄ S 
Published: July 2010

Summary
Helicobacter pylori-induced, in vitro stimulation of mononuclear cells was characterized by measuring DNA synthesis response, interferon-gamma (IFN-γ) secretion and the number of immunoglobulin-secreting cells. The strength of these responses was measured in 51 subjects comprising 36 dyspeptic patients from the Gastroenterological Unit and 15 members of the laboratory staff. Nineteen subjects had antibodies to H. pylori and 32 did not. The responses were compared with respect to H. pylori antibody status. Positive stimulation of DNA synthesis (stimulation index &gt; 2) was obtained in 96% of the subjects, and the bacterium induced IFN-γ secretion in all of them. The induction of immunoglobulin-secreting cells revealed B cell in vitro stimulation. The antibody-positive subjects had a tendency to synthesize less DNA (P not significant) and secrete less IFN-γ (P &lt; 0.05) in response to H. pylori than did the antibody-negative ones, but the differences were not marked. The results show that the whole H. pylori bacterium stimulates mononuclear cells. The nature of the stimulation is not yet characterized (non-specific versus specific).
Differential upregulation of intercellular adhesion molecule-1 in coeliac disease
Authors: STURGESS R P , MACARTNEY J C , MAKGOBA M W , HUNG C-H , HASKARD D O , CICLITIRA P J 
Published: July 2010

SummaryThe expression of intercellular adhesion molecule-l (ICAM-1) was studied on peroral jejunal biopsies from patients with coeliac disease. The biopsies from untreated patients exhibited greater staining of the superficial lamina propria cells compared with treated patients and controls. A gluten challenge in treated patients produced an altered staining pattern within 2 h. The results demonstrate the role of ICAM-1 expression in coeliac disease, providing further evidence for the role of lamina propria cells in the pathogenesis of this condition.
Lipopolysaccharide from Gram-negative bacteria enhances polyclonal B cell activation and exacerbates nephritis in MRL/lprmice
Authors: CAVALLO T , GRANHOLM N A 
Published: July 2010

SummaryDepletion of B cells in mice bearing the lymphoproliferation (Ipr) gene reduces lymphoprolifcralion and polyelonal B cell activation (PBA) and attenuates mononuclear cell vasculitis. We sought to verify whether the obverse was true. i.e. whether enhancement of B cell activity might exacerbate the nephritis of MRL /lpr( MRL) mice, a lupus-prone strain. The experimental approach was designed to address three questions: whether naturally occurring PBA in MRL mice could be further enhanced; whether enhanced PBA would exacerbate nephritis: and whether the mechanism of nephritis exacerbation involved interference with mononuclear phagocyte system (MPS) function. To enhance B cell activity, we injected MRL mice with lipopolysaccharide (LPS) from Gram-negative bacteria, a potent B cell activator. To determine whether nephritis was exacerbated, we performed immunopathologic studies and tests of renal function. To verify whether nephritis exacerbation involved impairment of MPS function, we probed the kinetics of immune complex removal from the circulation, their uptake by the liver and spleen, and their localization in kidney tissue. The results indicate that in MRL mice: (i) spontaneous PBA can be enhanced by LPS; (ii) enhancement of PBA by LPS exacerbates nephritis; and (iii) the MPS is already saturated, presumably due to excessive production of endogenous immune complexes. Thus, further increase in immune complex formation due to enhanced PBA by LPS results in increased localization of immune complexes in kidneys and exacerbated nephritis.
Early antibody responses in human schistosomiasis
Authors: EVENGÅRD B , HAMMARSTRÖM L , SMITH C I E , LINDER E 
Published: July 2010

SUMMARYEarly diagnosis is important when handling patients with acute schistosomiasis. This state is usually more severe in travellers and tourists than in the immune, resident patients. With increased travelling to areas endemic for schistosomiasis, a tool is needed to solve the problem of differential diagnosis due to the non-specific symptoms of the early stages of the disease. Early appearance of antibodies against excretory/secretory antigens of the intestinal tract in the adult worm was seen in six individuals recently infected with Schistosoma mansoni, using an indirect immunofluorescence technique. The antibodies were of IgM, IgG and IgA classes, and of the IgG1, IgG3 and IgA1 subclasses as detected by ELISA using an antigen preparation of adult worm. On immunoblots, using a freeze-dried adult worm antigen, IgG1 and IgG3 antibodies recognized antigens of 32–35 kD. Antibodies against these antigens could thus be a marker of early infection in previously non exposed visitors to endemic areas.
Cells and mediators which participate in immunoglobulin synthesis by human mononuclear cells. II. The mechanism of null cell participation in immunoglobulin synthesis and secretion by B cells
Authors: RICHTER M , TAYLOR S , MACPHAIL S , JODOUIN C A 
Published: July 2010

SUMMARYImmunoglobulins were synthesized and secreted by human B cells cultured with T cells with receptors for FcM (TM) helper cells, monocytes, null cells and PWM for 7 days. Immunoglobulin synthesis did not take place if the null cells were omitted from the cultures irrespective of the duration of the culture period. Null cells incorporated into the cultures at only 25% of their optimal concentration did not affect immunoglobulin synthesis markedly by the cultured B cells. However, the number of B cells in the culture could not be diluted without an accompanying marked reduction in immunoglobulin synthesis. The B cells synthesized and secreted significant quantities of immunoglobulin even when the null cells were added as late as day 6 of the 7-day culture whereas no or very little immunoglobulin was synthesized if the B cells were not present from the beginning of the 7-day culture. It was demonstrated that cultured null cells do not transform into B cells and do not attain their immunoglobulin-synthesizing function. Furthermore, cultured B cells do not transform into null cells and do not attain their helper function. The null cells can also be distinguished from the B cells on the basis of cell-surface markers, receptors, and blastogenic responsiveness to phytomitogens. It is concluded that (i) the human circulating B cells require the null cells, in addition to the TM cells, monocytes and PWM, in culture in order to synthesize and secrete immunoglobulin; (ii) the null cell signal that stimulates immunoglobulin synthesis and secretion by the B cells is probably the last signal following the TM helper cell, monocyte and PWM signals received by the B cells; and (iii) the null cells and the B cells constitute distinct lineages of cells.
Molecular size heterogeneity of immunoglobulins in health and disease
Authors: ROBERTS-THOMSON P J , SHEPHERD K 
Published: July 2010

SUMMARYThe molecular size of serum IgG, IgA and IgM in patients with a variety of monoclonal and polyclonal immune disorders has been determined by a sensitive immunoblotting technique. IgM, IgA and IgG3 paraproteins from patients with B cell lymphoproliferative disorders frequently polymerize with IgA paraproteins demonstrating two polymeric series, the basic unit of the more dominant series being monomeric IgA, and the second consists of a basic unit having a molecular mass of approximately 70 kD heavier than monomeric IgA. The molecular nature of this heavier IgA moiety was shown to be IgA covalently bound with a single moleculeof serum albumin or alpha anti-trypsin and this moiety was also observed in small quantities in sera from healthy subjects. IgM paraproteins, particularly from patients with malignant Iymphoproliferativc disorders, consisted of varying proportions of decamers, pentamers and monomers together with other low molecular weight IgM oligomers. Paraproteins from patients with benign conditions showed less tendency to exist in multiple molecular weight forms. Serum immunoglobulins from patients with polyclonal immune disorder also showed molecular sized heterogeneity. Significantly increased levels of dimeric IgA were observed in patients with alcoholic cirrhosis and Felty's syndrome, while low molecular weight IgM was commonly seen in patients with autoimmune disorders. In these latter disorders monomeric IgM correlated significantly with the serum IgM level suggesting a disorder of assembly of the IgM subunits during an ongoing IgM immune response. We have demonstrated considerable molecular size heterogeneity of serum immunoglobulins both in health and disease and have indicated some possible clinical associations.
Naturally occurring human IgG antibodies to intracellular and cytoskeletal components of human platelets
Authors: PFUELLER S L , LOGAN D , TRAN T T , BILSTON R A 
Published: July 2010

SUMMARYImmunoblotting of platelets that have been subjected to SDS-PAGE has revealed that sera from normal individuals contain IgG which binds to many platelet components. This binding was seen with autologous and heterologous platelets using serum of males and of nulliparous females who had not received blood transfusions. Although binding patterns of different sera were not identical, almost all sera caused IgG binding to platelet components of 87–90 kD, 140 kD (identified as vinculin) and 220–240 kD (tentatively identified as talin and actin-binding protein). Purified IgG showed the same binding pattern as whole serum and F(ab')2 fragments retained their ability to bind to many components. The titre of IgG binding in serum was 1:50–1600 while that of alloantibodies to the PIAI antigen was 1:3200. IgG binding components were not secreted when platelets were stimulated and were rarely associated with isolated membranes, but were located either in platelet cytoplasm or cytoskeletons, IgG binding was decreased by absorbing sera with lysed platelets or isolated cytoskeletons, but only slightly with intact platelets. Microaffinity purification of IgG which formed a major band on immunoblots showed that it was antibody with specificity for vinculin or its degradation products. These findings suggest that normal sera contain naturally occurring IgG antibodies with specificity for intracellular platelet antigens and that in some cases their titre approaches that of antibodies of pathological significance.
Depressed lymphocyte transformation and the role of prostaglandins in atopic dermatitis
Authors: JAKOB T , HUSPITH B N , LATCHMAN Y E , RYCROFT R , BROSTOFF J 
Published: July 2010

SUMMARYWe have shown that peripheral blood mononuclear cells (PBMC) from patients with atopic dermatitis have a reduced in vitro proliferative responsiveness to concanavalin A when compared with non-atopic controls, Addition of the cyclo-oxygenase inhibitor indomethacin caused a significant enhancement of the mitogen response in the patients, indicating a suppressive effect of cyclooxygenase products. We have further demonstrated increased levels of prostaglandin E2 in the supernatants of the PBMC cultures and mereased levels of IgE immune complexes in the sera of the aotpic dermatitis patients and therefore hypothesize that IgE immune complexes may cause increased monocyte production of prostaglandins which in turn appears to be responsible for a reduced lymphocyte proliferation.