bluuebunny/crossref_metadata_2025_split huggingface dataset:
Anaplasmosis in Uganda. II. Prevalence of Bovine Anaplasmosis
Authors: SSENYONGA G. S. Z. , KAKOMA I. , MONTENEGRO‐JAMES S. , NYEKO P. J. , NANTEZA A. , BUGA R. 
Published: July 2006

The prevalence of bovine anaplasmosis was studied in 320 Zebu cattle randomly selected from three regions of Uganda (central, south‐western and north‐western) using DOT‐ELISA, Western immunoblotting. Rapid Card Agglutination Test (RCAT), Capillary Tube Agglutination Test (CAT), Complement Fixation Test (CFT), and parasitological techniques. Dried blood on Whatman filter paper no. I was eluated in PBS 0.05% Tween 20 prior to testing at an initial dilution of 1:25.The incidence of parasitaemia ranged from 25% in the central region to 35% in the northwestern region and the serological prevalence was lower in the central region and highest in the north‐west. Prevalence rates assayed by DOT‐ELISA and Western immunoblotting were 1.5‐fold greater than those tested with RCAT and 3‐fold greater than in CAT. The overall prevalence rates by DOT‐ELISA and Western immunoblotting compared favourably with CFT data.The present data utilizing dried blood on filter papers indicate that there is a high prevalence of anaplasmosis in those regions of Uganda surveyed and it confirms our observations and those of others that collecting blood on filter papers is a suitable technique for large‐scale screening and for seroepidemiological studies.
Infiltrating Neutrophils Differ from Circulating Neutrophils when Stimulated with C5a, NAP‐l/IL‐8, LTB4 and FMLP
Authors: MROWIETZ U. , SCHRÖDER J.‐M. , BRASCH J. , CHRISTOPHERS E. 
Published: June 2006

In this study we report on functional characteristics of pustule as well as blood polymorphonuclear neutrophils (PMN) in patient suffering from relapsing bullous staphyloderma. Large numbers of viable PMN from newly formed pustules as well as from the peripheral blood were investigated. During the course of disease chemotactic migration, enzyme degranulation, superoxide‐anion generation and leukotriene B4 production were determined simultaneously.The results revealed C5a‐ and NAP‐1/IL‐8‐specific dysfunction of pustule PMN as compared with blood PMN. In contrast, FMLP‐elicited functional activities of pustule PMN were only slightly affected.Our findings provide evidence that in inflamed tissue invading PMN are regulated by in situ generated mediators. C5a produced by staph. aureus‐induced activation of the alternative pathway of the complement cascade represents predominant regulatory factor in situ. Furthermore, the results substantiate previous observations concerning different modulation of C5a and f‐met‐peptide receptors on human PMN.
A Study of Donor Alloreactivity, which may predict Acute Graft‐Versus‐Host Disease in HLA Identical Bone Marrow Transplantations for Early Leukaemia
Authors: JOHNSEN H. E. , BOSTROM L. , MOLLER J. , JORGENSEN J. A. , JENSEN L. , RINGDEN O. 
Published: June 2006

Recent studies performed in Seattle, USA have suggested that pretransplant assignment of high or low donor alloreactivity may predict acute graft‐versus‐host disease (aGvHD) after allogeneic HLA identical marrow transplantation for acute leukaemia. The effect of such pretrunsplant assignment was studied in a Scandinavian population of 114 consecutive transplantations for acute and chronic leukaemias in 1st remission (n= 74) or chronic phase (n= 40) performed between 1975 and 1989.The selected cut‐off value for discriminating between donors of high and low responding capacity (DRC) was based on distribution plots of results from the pretransplant mixed lymphocyte culture (MLC) and chosen as the median value (80% normalized response). Then 57 donors were assigned with high DRC and 57 donors assigned with low DRC. Kaplan‐Meier estimates of the probability of patients to develop Grade M or higher aGvHD in receipt of high or low responder donor transplants were compared by univariant analysis. The patients in first remission or chronic phase transplanted with bone marrow from donors assigned as high or low responders had a 36.1% and 10.6% risk for aGvHD, respectively, a difference found to be significant by log rank test (chi‐squared = 10.1, d.f.= 1, P= 0.0015).Subsequent studies of the cellular and humoral requirements for this predictive response of donor cells, by blocking with cytokine specific antibodies, addition of excess of recombinant human cytokines and scanning of lymphocyte subsets during the response, showed that the response against pool cells mostly depended upon IL‐2 responding cells with the phenotype CD3+, CD4+, CD8‐, CD25+, CD16‐.It is concluded that prospective studies of alloreactivity as a risk factor should be performed to confirm the above findings,
From Pathology to Physiology of the Human T‐Lymphocyte Receptor
Authors: REGEIRO J. R. , TIMÓN M. , PÉREZ‐ACIEGO P. , CORELL A. , MARTÍN‐VILLA J. M. , RODRÍGUEZ‐GALLEGO C. , GÓNGORA R. , ARNAIZ‐VILLENA A. 
Published: June 2006

SummaryThe recent description of a selective human CD3γ deficiency and other T‐cell receptor (TCR)/CD3 structural and functional defects, together with previous biochemical data on the structure and interactions of the TCR/CD3 complex, may aid in elucidating the physiology of this multi‐subunit membrane ensemble. CD3γ seemed to be required for the commitment and thymic maturation of an important fraction of T lymphocytes to the CD8 (but not CD4) lineage, perhaps by participating with the CD8 co‐receptor in the instructive signal delivered throtigh the αβ TCR during intrathymic positive selection by HLA class I molecules. The homologous CD3δ component would, in contrast, be necessary for the selection of CD4 lymphocytes by HLA class II molecules. The interaction of CD4 and CD8 with the TCR/CD3 complex during antigen recognition may thus be asymmetrical, taking place through CD3δ and γ respectively. Also, the existence of in vivo functional TCR/CD3 hemireceptors (lacking either CD3γ or CD3δ is suggested, and defects in their relative amount on the T‐cell surface may disrupt unresponsiveness to self antigens and generate autoimmunity.
T‐Cell Epitopes on the Human Acetylcholine Receptor α‐Subunit Residues 10‐84 in Myasthenia Gravis
Authors: ÅHLBERG R. , YI Q. , ENG H. , PIRSKANEN R. , LEFVERT A. K. 
Published: June 2006

In myasthenia gravis the production of anti‐acetylcholine receptor antibodies is modulated by acetylcholine receptor‐specific T cells. Most B‐and T‐cell epitopes are located on the α‐subunit of the receptor. In order to map the fine specificity of the antigen‐specific T cells in myasthenia gravis, T‐cell stimulation in response to 70 hexapeptides was studied in 24 patients and 24 healthy individuals. The hexapeptides overlapped with one amino acid and represented residues 10‐84 of the NH2‐terminal part of the α‐subunit of the receptor. The IFN‐γ secretion from single T cells was used to detect T‐cell stimulation.A significanl difference in the T‐cell response to several of the peptides was found between patients and healthy controls. The majority of the hexapeptides induced T‐cell stimulation in at least one of the patients. Peptidc‐induced T‐cell stimulation was evident in all but one of the patients. The results indicate that different epitopes and multiple T‐cell clones are involved in the T‐cell recognition of the acetylcholine receptor.
C3bi/CR3 is a Main Ligand‐Receptor Interaction in Attachment and Phagocytosis of C3‐Coated Particles by Mouse Peritoneal Macrophages
Authors: KIMURA M. , GRIFFIN F. M. 
Published: June 2006

We investigated the relative role of C3bi‐CR3 interaetion in the binding and phagocytosis of EAC43 by mouse peritoneal macrophages. Anti‐Mac‐1 F(ab′)2 markedly inhibited the binding and lymphokine‐induced phagocytosis of both EAC43b and EAC43bi, Fifty per cent inhibition of attachment and phagocytosis occurred at 1 μml of anti‐Mac‐1 F(ab′)2 in the incubation media. On the other hand, ElgG binding and phagocytosis were not inhibited at all even at a concentration of 10 μ/ml. Depletion of divalent ealions from the incubalion media abolished EAC43b and EAC43bi rosettes but not ElgG rosettes or phagocytosis. These data suggested that both EAC43b and EAC43bi binding to macrophages were mediated via CR3.Because a drastic decrease of FAC43bi rosettes was observed in the case of EAC43bi cells prepared with smaller amounts of C3, a small eontamination of C3bi molecules on EAC43b, itself, cannot explain the efficient attachment of EAC43b, We propose that EAC43b on the macrophage surface can be quickly converted to EAC43bi, forming EAC43bi rosettes, and that those erythrocytes are vigorously ingested by lymphokine‐activated macrophages. In accordance with this hypothesis, we demonstrated that EAC43b was converted to E AC43bi in the medium in whicb macrophages had been ineubated
Effect of Mucosal and Systemic Immunization with Pneumococcal Polysaccharide Type 3, 4 and 14 in the Rat
Authors: VAN DEN DOBBELSTEEN G. P. J. M. , BRUNEKREEF K. , SMINIA T. , VAN REES E. P. 
Published: June 2006

Four immunization routes were investigated to induce an immune response against three structurally different types of pneumoccoccal polysaccharide (PPS) in the rat. In particular, the contribution of the IgA isotype in these immune responses was studied. Six days after administration of PPS type 3, 4 or 14. the localization of specific antibody‐containing cells (ACC) in different lymphoid tissues and the antibody titres in serum were studied.All four routes induced anti‐PPS ACC in the spleen. After intraduodenal, intravenous and especially intraperitoneal administration of PPS, many IgA‐specific anti‐PPS ACC were also found in parathymic and mesenteric lymph nodes and in the lamina propria of intestinal tissue. Several anti‐PPS ACC were found in Peyer's patches, located peripheral of the B‐cell areas. The intratracheal immunization elicited only a local immune response, in bronchus‐associated lymphoid tissues and paratracheal lymph nodes. The localization of these anti‐PPS ACC was influenced by the route of immunization.After all four investigated routes, specific antibodies were found in serum against PPS. However, some remarkable differences between PPS‐3, 4 and 14 were found in the magnitude of the immune response and the distribution of the isotypes. Both route of immunization and structure of the PPS have a profound influence on the immune responses in rats.
Complement Receptor Type 2 Mediates Infection of the Human CD4‐Negative Raji B‐Cell Line with Opsonized HIV
Authors: BOYER V. , DELIBRIAS C. , NORAZ N. , FISCHER E. , KAZATCHKINE M. D. , DESGRANGES C. 
Published: July 2006

Boyer V, Delibrias C, Noraz N, Fischer E, Kazatchkine MD, Desgranges C. Complement Receptor Type 2 Mediates Infection of the Human CD4‐Negative Raji B‐Cell Line with Opsonized HIV. Scand J Immunol 1992;36:879‐83Opsonization of the HTLV‐RF and HTLV‐IIIB strains of HIV‐1 with normal human HIV seronegative serum under conditions that allow complement activation resulted in the productive infection of cells of the Raji B lymphoblastoid cell line. Under the same experimental conditions, no infection of Raji cells was observed with unopsonized virus. Infection of Raji cells with complement‐opsonized HIV‐1 was totally suppressed by preblocking the function of CR2 (the C3dg receptor, CD21) on the cells with a monoclonal anti‐CR2 antibody cross‐linked with rabbit F(ab')2 anti‐mouse immunoglobulin antibodies. Infection of Raji cells occurred independently of CD4 since the cells lacked the expression of CD4 antigen and of CD4 transcripts. Thus, Raji cells may be infected with complement‐opsonized HIV independently of CD4 and in the absence of antibodies. By mediating and/or enhancing HIV infection, complement and complement receptors contribute to extend the range of target cells to the virus and may increase infection in patients with a low viral load.
Antigen‐Specific Increases in the Number of Splenocytes Expressing MHC Class II Molecules Following Restimulation with Antigen in Various Physical Forms
Authors: BERGSTRÖM‐MOLLAOGLU M. , LÖVGREN K. , ÅKERBLOM L. , FOSSUM C. , MOREIN B. 
Published: June 2006

To understand how a presentation system for antigens initiates an immune response and why it has a strong adjuvant activity, a number of parameters need to be analysed. In this study the frequency of spleen cells expressing MHC class II (Ia antigen) was determined after immunization of mice and restimulation of their spleen cells, in vitro, with influenza virus envelope proteins in different physical forms, namely iscoms, micelles and virus particles.All three forms of the antigen stimulated, in an antigen‐specific manner, an increased proportion of spleen cells expressing MHC class II in the restimulation experiments. The induction of increased MHC class II expression was at least partly dependent on antigen‐specific indction of IFN‐γ sinec anantibody to IFN‐γ partly inhibited the increase of MHC classII+ cells induced by iscom or by Concanavalin A. The iscom‐borne antigens were superior to micelles to prime the immune response in vitro, indicating a capacity to induce memory cells. This primed immune response was readily recalled in vitro, as measured by IFN‐γ production and an increased number of MHC class II positive cells.
Recombinant Human Tumour Necrosis Factor‐α (rhTNF‐α) and rhTNF‐α Analogue Enhance Amyloid Deposition in the Syrian Hamster
Authors: NIEWOLD Th. A. , GRUYS E. , ARAKAWA T. , SHIRAHAMA T. , KISILEVSKY R. 
Published: July 2006

Tumour necrosis factor‐α (TNF‐α) is one of the cytokines that stimulate the production of serum amyloid A (SAA), the precursor of AA amyloid. The role of TNF‐α in amyloidogenesis was investigated in experimental hamsters using purified recombinant human TNF‐α (rhTNF‐α) and rhTNF‐α analogue different from the normal molecule by two amino acid substitutions. Daily injections of 1 μg rhTNF‐α resulted in elevated SAA levels but even in the presence of amyloid enhancing factor (AEF) no amyloid was deposited, indicating that apart from the AEF and one particular SAA stimulating factor an additional factor is needed to result in amyloid deposition. This factor is generated by repeated injections of E. coli lipopolysaccharide (LPS).A single intraperitoneal injection of 12,5 μg or more of rhTNF‐ä followed by seven daily subcutaneous injections of LPS resulted in enhanced amyloid deposition. Heat denaturation of rhTNF‐α did abolish its AEF activity. The rhTNF‐α analogue, having one‐fifth of the cytotoxic activity of the normal rhTNF‐α, showed a similar reduction in its SAA‐inducing capacity and its amyloidogenicity. This suggests the AEF activity to be closely related to TNF‐α activity. However, poly(I)poly(C) (a potent inducer of IL‐6) also showed AEF activity, suggesting that not a single cytokine but rather a certain combination of different cytokines could be decisive in AA amyloidogenesis.
Test for Ability of Decay‐Accelerating Factor (DAF, CD55) and CD59 to Alleviate Complement‐Mediated Damage of Xeno‐Erythrocytes
Authors: MIYAGAWA S. , SHIRAKURA R. , MATSUMIYA G. , NAKATA S. , MATSUDA H. , HATANAKA M. , MATSUMOTO M. , KITAMURA H. , SEYA T. 
Published: July 2006

We investigated the susceptibility to human complement (C) of xeno‐erythrocytes into which phosphatidylinositol (PI)‐anchored human C regulatory protein, decay‐accelerating factor (DAF) or CD59 had been incorporated. Erythrocytes of sheep (Esh), swine (Esw), dog (Edg), and guinea pig (Egp), unsensitized with human natural antibody (Ab), were used as xeno‐target. C‐mediated lysis of erythrocytes (E) was induced in both classical and alternative pathways in parallel with the density of the sensitized Ab, except for Egp. The efficacy of DAF/CD59‐mediated protection of the xeno E from human C, however, differed among these E species. In both classical and alternative pathways, Esh or Esw, which are non‐activator surfaces, were protected by the incorporated DAF or CD59, DAF being more effective than CD59. On the other hand, CD59 was more effective than DAF in both pathways in protection of Egp, which is an alternative pathway activator.To elucidate this different behaviour of DAF and CD59, C3 step inhibition by the incorporated DAF or CD59 was measured. DAF was effective in the suppression of classical pathway‐mediated C3 deposition in Esh, Esw and Egp, but not in Edg, while CD59 exhibited negligible effects in this regard. Next, inhibition of the lysis by CD59 was tested by haemolytic assay. CD59 did not block the C5b‐8‐mediated lysis in any xeno E. It also barely blocked C5b‐9‐mediated lysis, except in the case of Egp, in which CD59 partly blocked C9 attack. Membrane constituents on targets other than the incorporated complement inhibitors may be a crucial factor in the induction of cytolysis and, presumably, in hyperacute rejection.
In Vivo Depletion of Chicken T‐Cell Subsets
Authors: CIHAK J. , LÖSCH U. , HOFFMANN‐FEZER G. , CHEN C. H. , COOPER M. D. , ZIEGLER‐HEITBROCK H. W. L. 
Published: July 2006

In the chicken three types of T‐cell receptors can be defined by monoclonal antibodies TCR1, TCR2 and TCR3, which recognize γδ T cells, and Vβ1‐ and Vβ2‐expressing αβ T cells, respectively. In the present report we have analysed means of selectively depleting the γδ T cells and the Vβ1 +αβ T cells.γδ cells, which represent up to 66% of all T cells in blood of a 6‐month‐old chicken, can be effectively depleted by neonatal thymectomy (Tx) to levels as low as 1%. Immunohistology demonstrates a similar depletion in lymphoid organs while intestinal epithelium‐associated γδ T cells are affected by Tx to a lesser extent.Vβ1‐bearing αβ T cells, which comprise about 80% of the αβ T cells, were depleted by embryonic and neonatal injection of the TCR2 antibody. In the thymus such treatment depleted only the Vβ1 +αβ T cells with high density expression of T‐cell receptor. Therefore, we thymectomized TCR2‐treated animals in order to prevent development of mature Vβ1+αβ T cells from the low density immature thymocytes. Treatment of chickens with a total of 22 mg of TCR2 antibody plus Tx reduced Vβ+αβ T cells from an average of 65% to 10% of all T cells. In these TCR2 antibody‐treated animals the Vβ2‐expressing αβ T cells become the predominant type of T cell (average 85%).
Murine APC Activation in the Xenogeneic MLC
Authors: BENFIELD M. R. , WITSON J. C. , ALTER B. J. , BACH F. H. 
Published: July 2006

Purified human T cells proliferate in response to direct and indirect presentation of human alloantigens. However, until recently it was believed that human T cells could respond only indirectly to murine xenoantigens. We recently used the mixed leucocyte culture (M LC) to demonstrate that purified human T cells proliferate in response to direct presentation of murine xenoantigens by murine antigen‐presenting cells (APC) in the presence of human cytokines. We suggested that cytokines might function poorly across species barriers.In this study, we demonstrate that although proliferation occurs in the presence of exogenously added cytokines, the precursor frequency of responding human T cells is much lower in a xenogeneic than in an allogeneic MLC. We demonstrate that human T cells also proliferate in response to murine APC in the presence of murine cytokines, and murine cytokines augment the proliferative response seen in a human anti‐human MLC, ruling out the possibility that an absolute cytokinc incompatibility exists between these species. We show that exogenously added human IL‐1 causes maximal proliferation of human T cells in response to murine xenoantigens only when added early in the culture. We further demonstrate that murine APC preincubatcd in human rIL‐1, and washed extensively, prior to use as stimulating cells, cause human T‐cell proliferation without the need for exogenously added cytokines. Finally, we noted that during interactions of human T cells and murine APC, little to no IL‐1 is produced, whereas after the addition of exogenous IL‐1, a marked increase in the production of IL‐1 is seen. These data suggest that during interactions between human T cells and murine APC, the murine cells do not receive adequate stimulation to produce sufficient costimulatory signals to allow proliferation of the human T cells.
Imbalance of the CD4+ Subpopulations Expressing CD45RA and CD29 Antigens in the Peripheral Blood of Adults and Children with Down Syndrome
Authors: BARRENA M. J. , ECHANIZ P. , GARCIA‐SERRANO C. , CUADRADO E. 
Published: July 2006

Peripheral blood lymphoid subsets expressing either CD45RA or CD29 antigens, were quantified in 30 children and 59 adults with Down Syndrome and appropriate age‐matched controls, by dual immunofluorescence and flow cytometry, Down's patients, both adults and children, displayed a significant decrease of CD4+CD45RA+ cells in comparison with the observed in their age‐matched controls, but no difference was found in the CD4+CD29+ subset. These results show clearly the imbalance of these subpopulations in the peripheral blood of individuals with Down syndrome that result in the inversion of the CD45RA/CD29 ratio, due to a major reduction of the CD45RA subset. No obvious diflerence was found in the CD45RA/CD29 ratio within the CD4 negative cells.Abnormalities of these subpopulations could be indicative of early senescence of the immune system, since age‐related changes in Down's persons were in parallel with those observed in normal individuals and the proportion of both subpopulations were roughly similar in Down's children and normal adults.
Histocompatibility Complex Gene Products and Exposure to Oestrogen: Two Independent Disease Accelerating Factors in Murine Lupus
Authors: CARLSTEN H. , TARKOWSKI A. 
Published: July 2006

A number of studies have demonstrated that oestrogen exerts a significant impact on the course of experimental autoimmune diseases. Exposure to oestrogen aggravates SLE glomerulonephritis whereas the opposite outcome has been demonstrated in experimental arthritis, vasculitis, thyroiditis, and sialadenitis. In this report we have analysed the respective impact of H‐2z linked gene products and long‐term treatment with physiological doses of oestradiol on clinical and immunological variables in castrated backcrosses of lupus prone NZB/W and NZB mice.Our results demonstrate that H‐2z linked gene products accelerate B‐cell activation and stimulate autoantibody production resulting in aggravation of glomerulonephritis and precocious death in renal failure. These H‐2z linked gene products do not influence T‐cell mediated sialadenitis. Irrespectively of the H‐2 haplotype of the mice, administration of oestrogen resulted in intense polyclonal B cell activation and aggravation of glomerulonephritis. However, exposure to oestrogen resulted in amelioration of sialadenitis. Notably, our result indicates that B‐cell activation achieved by oestrogen and H‐2z gene linked products, respectively is mediated by independent mechanisms.In addition, we have developed a predictive in vivo test that permits forecasts regarding efficiency of oestrogen treatment for suppression of T‐cell mediated lesions. Using this test procedure in young, clinically healthy SLE mice we have been able to prove that animals displaying suppressed delayed type hypersensitivity (DTH) after short‐term oestrogen exposure showed significantly lower long‐term morbidity regarding development of sialadenitis upon continuous treatment with physiological doses of oestradiol.