bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inhibition of Neutrophil Chemotaxis by Elastase‐Generated IgG Fragments
Authors: ECKLE I. , KOLB G. , HAVEMANN K. 
Published: June 2006

IgG1 is cleaved in vitro by granulocyte elastase into Fc and Fab fragments. The elastase‐specific Fe fragment has been previously detected in vivo. Biological activity of the fragments has been described in modulating neutrophil oxidative metabolism and enzyme release. To investigate further effects granulocyte chemotaxis(CT) was tested. The CT was assayed in Boyden chambers and the chemotactic index (CI) was calculated which represents the mean distance travelled by the activated cells.Stimulation of leucocyte CT by casein, activated scrum and FMLP gives maximal values of Δ CI = 46.7, 26.4 and 7.1 μm, respectively. Native IgG1 and the elastase‐produced IgG fragments do not stimulate leucocyte CT.FMLP‐stimulated CT is specifically inhibited by the elastase‐produced Fc fragments. Addition of 7 nmol Fc to stimulus concentrations of 16 to 125 nM FMLP results in total inhibition of chemotaxis demonstrated by CI values which are lower than those for unstitmulated cells. The inhibition of CT is concentration dependent in the range of 2 to 7 nmol Fc/106PMN.Number and affinity of FMLP receptors are not incipience by Fc fragments, so Fc binds neither to FMLP nor the FMLP receptor.CT stimulated by casein shows a large portion of chemokinesis. Only at suboptimal casein concentrations do Fc and IgG have an Inhibitory effect on CT (0.63 mg casein /ml. 10 nmol peptide/106 PMN).C5a‐stimulaicd CT is not influenced by IgG or IgG fragments which indicates that the samples are not cytotoxic. So the FMLP and casein‐stimulated CT is specifically inhibited by the elastase‐produced Fc fragments in a low concentration range.
What Determines an Antigen‐Specific IgE Isotypic Response?—A Hypothesis
Authors: Chen Swey‐Shen Alex 
Published: June 2006

SummaryTwo models to account for an antigen‐specific IgE isotypic response are proposed. Both models assume a first‐tiered IgE production induced by antigen and IL‐4; however, the processed IgE or Ag IgE immune complexes stimulate Tɛ cells differently in the two models. In Model I. we propose that Tɛ cells express conventional T‐cell receptors which recognize IgE isotypic determinants. Model IA proposes that IgE fragments are processed and recognized along with class II MHC molecules, and Tɛ cell preferentially act on antigen‐activated IgE‐committed Tɛ cells via recognition o! processed membrane IgE determinants but not antigens; thus Tɛ cells are in principle capable of modulating non‐antigen‐specific polyclonal IgE responses. Model IB proposes that IgE function as a class‐restriction determinant for nominal antigens analogous to that of class II molecules, and Tɛ cells exert stringent antigen‐specific IgE isotypic responses by recognizing nominal antigens restricted to IgE, Tɛ cells thus exert antigen‐specific and IgE concerted immunoregulation. and do not participate in modulating polyclonal IgE production. Model II proposes a heterotypic interaction of IgE with a cell interaction receptor (or IgE Fc receptor) on T cells, Tɛ cells modulate antigen‐specific IgE isotypic responses via ligation with IgE antigen immune complexes on B‐cell surface; thus. Tɛ cells in principle contribute to polyclonal IgE responses.
Dietary Antigen Handling by Mother and Offspring
Authors: TELEMO E. , BATLEY M. , MILLER B. G. , STOKES C. R. , BOURNE F. J. 
Published: June 2006

Sows were Ted ovalbumin (OvA) as a novel protein antigen either throughout gestation and lactation (G + L) or during tactation only (L). This resulted in a significant uptake of OvA into blood, colostrum and milk along with a specific IgG response. In piglets from the G + L group. OvA and antibodies to OvA were detected in serum after ingestion of colostrum. In a large proportion of these piglets OvA was still detected at 3 weeks of age. In she L group a significant proportion of the piglets responded to OvA whilst still suckling their mother.At 3 weeks of age all piglets were weaned onto an egg‐based diet. A similar uptake of OvA was seen in all piglets but there was no response to OvA in the G + L piglets. In piglets from sows fed only during lactation, however, a rapid IgG anti‐OvA response and signs of diarrhoea were seen.The results suggest that factors of immunological importance are passed over from mother to offspring and it is proposed that immunological experience of dietary antigens by the mother is important for a 'safe’tolerance induction in her offspring.
Phagocytosis of β‐1,3‐D‐Glucan‐Derivatized Microbeads by Mouse Peritoneal Macrophages Involves Three Different Receptors
Authors: KONOPSKI Z. , RASMUSSEN L.‐T. , SELJELID R. , ESKELAND T. 
Published: June 2006

Intraperitoneal injection of β‐1,3‐D‐glucan coupled to the surface of monodisperse methacrylate microbeads improves the resistence against bacterial infections in mice, while methacrylate microbeads alone do not. The effect of the glucan‐derivatized microbeads (GDM) is considered lo be mediated through peritoneal macrophages [34, 40].We show that both GDM and (he underivatized methacrylate microbeads (UDM) treated with normal serum were rapidly bound and phagocytozed by mouse peritoneal macrophages in vitro. We found that both complement and fibronectin opsonized the bead.‐; and were responsible for the uptake.Treatment of microbeads with serum lacking fibronectin and complement activity still gave BOOK uptake of GDM, but not uptake of UDM. The uptake of GDM was similar to the uptake of untreated GDM and was inhibited by pretreatment of macrophages with soluble β‐1,3‐D‐gluean.Our conclusion is that GDM and UDM intraperitoneally bind fibronectin and C3 through activation of the alternative pathway of complement. This leads to their phagocytosis by macrophages through fibronectin and complement receptors. GDM are also internalized via β‐glucan receptors. We present the hypothesis that the β‐glucan receptors on peritoneal macrophages account for the protective effect of GDM in intraperitoneal bacterial infections.
Serum Amyloid A Isoforms in Inflammation
Authors: RAYNES J. G. , McADAM K. P. W. J. 
Published: June 2006

Serum amyloid A protein (SAA) was extracted from serum using hydrophobic interaction chromatography and four or six isoforms were separated by isoelectric‐focusing. These represented three pairs of isoforms, each with and without an N‐terminal arginine. SAA I (pi 6.1). SAA l des‐arg (pl 5.9). SAA2α (pi 6.9) and SAAα: des‐arg (pl 6.6) were found to be present in all individuals from Europe and the USA. A minority of these individuals (11 of 56) expressed SAA2/β (pl 7. 1) and SAA2/β des‐arg (pi 6.8).Serum from patients in Papua New Guinea and Malawi both showed a much higher frequency ofSAA2/β. There was no indication of altered isoforms in regions with high incidence of reactive AA amyloidosis. In sequential serum samples, concentrations of des‐arg isoforms were found to reach a maximum 0 24 h later than isoforms with an arginine. Concentrations of the isoform SAA1 decreased faster in five of six patients (16±:7.5 h to decrease 50%) than SAAl des‐arg (22± 11 h to decrease 50%). Variations in the handling of N‐terminal arginine may be important for the formation‐susceptibility of amyloid deposits.
Expression of CD26 (Dipeptidyl Peptidase IV) on Resting and Activated Human T‐Lymphocytes
Authors: MATTERN T. , SCHOLZ W. , FELLER A. C. , FLAD H.‐D. , ULMER A. J. 
Published: June 2006

CD26 is an activation antigen which is expressed on the surface of human T‐lymphocytes. It has been characterized to be the dipeptidyl peptidase IV (DPP IV). Considerable amounts of CD26 are already present on resting T‐lymphocytes. The expression of CD26 is enhanced by T‐cell milogens or antigens. A correlation of CD26 expression and of enhanced enzymatic activity was observed after T‐cell activation. Our data indicate that not only the immunoreactivity, but also the enzymatic activity of CD26 are detectable on the cell surface. In addition, de novo expression of CD26 was demonstrated on CD26‐negative T‐cells after mitogenic or antigenic stimulation.CD26 expression is initiated during the G1 phase of the cell cycle. The expression occurs nearly simultaneously with HLA‐DR, but later than CD25. Similar lo CD25 and HLA‐DR, CD26 is not a permanent marker on the surface of T‐lymphocytes, but is down‐regulated after 7 days of culture. When testing the influence of interleukin I, interleukin 2, tumour necrosis factor, and interferon‐γ on the expression of CD26, no effect was found on unstimulated or on mitogen‐stimulated T‐lymphocytes. The binding of two different monoclonal antibodies against CD26 (anti‐DPP IV and anti‐Tal) to resting and activated T‐lymphocytes revealed a different pattern of immunoreactivity. Resting T‐lymphocytes reacted stronger with anti‐DPP IV than with anti‐Ta I. However, binding of the two monoclonal antibodies to T‐cell blasts did not show significant differences. These data indicate that CD26 may be expressed in differently modulated configurations on the surface of T‐cells, which may be associated with a distinct status of activation and or function.
Tumour Necrosis Factor B Gene Polymorphism in Relation to Complotype in Couples with Spontaneous Abortions and in Control Families
Authors: LAITINEN T. , LOKKI M.‐L. , TULPPALA M. , YLIKORKALA O. , KOSKIMIES S. 
Published: June 2006

Nco I restriction fragment length polymorphism (RFLP) of the tumour necrosis factor B (TNFB) gene gives two allelic fragments of 5.5 and 10.5 kb, corresponding to the TNFB*1 and TNFB*2 alleles, respectively.The frequencies of these alleles were analysed in 121 healthy Finns and 56 Finnish couples suffering from recurrent spontaneous abortions (RSA). In the healthy Finns the frequency of TNFB*1 was 37% and that of TNFB*2 63%, of which the frequency of TNFB*1 was significantly increased compared with the Danish population. No deviation was seen between the RSA couples and the Finnish controls.TNF genes are located in major histocompalibility complex class III region close to complement (BF, C4A and CAB) genes. Some complotypes associated most often with the TNFB*1 (S01, S30, S02) and some (S31, F320) with the TNFB*2 allele in the healthy Finns.The combination of the TNFB and the C4 ‘null’ allele differed between the RSA couples and the Finnish controls.
Cyclosporine A in Fat Emulsion Carrier: Immunosuppressive Effect In Vitro
Authors: TIBELL A. , RINGDÉN O. , SUNDBERG B. 
Published: June 2006

We have recently shown in a rut model that the acute decrease in glomerular filtration rate caused by intravenous Sandimmun® can be avoided if Cyclosporine A (CyA) is given in a fat emulsion carrier instead. The present study was undertaken to determine the immunosuppressive effect in vitro of this new formulation.The inhibitory effect on the lymphocyte responsiveness of CyA in fat emulsion carrier was compared with that of CyA dissolved in alcohol, using mitogens as well as alloantigens as stimuli. In the mixed lymphocyte culture and cell‐mediated lympholysis tests and in the interleukin‐2 assay, both formulations seemed equally effective. CyA in fat emulsion was somewhat less effective than CyA in alcohol in the mitogen tests. In clinical practice the fat emulsion would be rapidly metabolized, and to further evaluate our new formulation, studies in experimental Organ transplantation are needed.
Invertebrate Immunity: Another Viewpoint
Authors: Cooper Edwin L. , Rinkevich Baruch , Uhlenbruck Gerhard , Valembois Pierre 
Published: June 2006

SummaryAll vertebrates and invertebrates manifest self/non‐self recognition. Any attempt to answer the question of adaptive significance of recognition must take into account the universality of receptor‐mediated responses. These may lake two forms: (1) rearranging, clonally distributed antigen‐specific receptors that distinguish in the broadest sense between self and non‐self, and non‐self A from non‐self B, latecomers on the evolutionary scene; (2) pattern recognition receptors, the earliest to evolve and still around, necessitating the requirement for induced second signals in T‐ and B‐cell activation. Either strategy need not force upon invertebrates the organization, structure and adaptive functions of vertebrate immune systems. Thus, we can freely delve into the unique aspects of the primitive immune mechanisms of invertebrates. In contrast, using the opposite strategy which is still problematic, i.e. linking invertebrate and vertebrate defence, seems to give us an approach to universality that might eventually reveal homologous kinship.
Nearly Identical T‐Cell Receptor V‐Gene Usage at Birth in Two Cohorts of Distinctly Different Ethnic Origin: Influence of Environment in the Final Maturation in the Adult
Authors: RAMAKRISHNAN N. S. , GRUNEWALD J. , JANSON C. H. , WIGZELL H. 
Published: June 2006

We have previously analysed the T‐cell receptor (TCR) V‐gene usage in peripheral blood T lymphocytes from a group of healthy Scandinavians, and described a biased representation (i.e. a statistically significant higher median representation) for some of the TCR V genes towards the CD4+ subpopulation. In a subsequent study the usage of the same V genes was analysed in single positive (CD4+CD8− and CD4−CD8+) human thymocytes, and a similar type of skewness was noted. These observations might be explained by an influence of the specificity of the TCR of thymocytes on the maturation into the CD4+ or the CD8+ lineage. Such a model would assume an interaction between a common determinant on the major histocompatibility complex (MHC) class I or class II molecules, or with a peptide that is preferentially presented by either of the two molecules, and the TCR on the maturing thymocyte. To investigate the possible influence of a different genetic background and environment on skewed TCR V‐gene representation, we have in this study analysed the TCR V‐gene usage in peripheral blood and umbilical cord blood lymphocytes obtained from Asians, with a different ethnic and environmental background from our previous Scandinavian subjects. In the umbilical cord blood lymphocytes the TCR V‐gene usage was close to identical between the two different ethnic groups in both CD4+ and CD8+ subpopulations. Analysing the peripheral blood lymphocyte (PBL) TCR V‐gene usage, we found that three of the four monoclonal antibodies (MoAb) with a biased reactivity towards the CD4+ subpopulation in the Scandinavian group also showed a similar skewed reactivity in this study. Thus, the majority of the TCR V genes were used in a similar way. Some minor but definite disrepancies could be detected when comparing ICR V‐gene usage in adult individuals from these two different ethnic groups. These differences could be inferred to be due to selective peripheral expansion through environmental pressure of T cells utilizing a specific Vβ gene segment.We conclude that a striking preservation of biased TCR V‐gene usage does exist in humans of distinctly different ethnic origin.
Over‐Estimation of the Number of Complement Receptor Type 1 (CR1) on Erythrocytes
Authors: QUADRI R. A. , SCHIFFERLI J. A. 
Published: June 2006

Quadri RA, Schifferli JA. Over‐Estimation of the Number of Complement Receptor Type I (CR1) on Erythrocytes. Scand J Immunol 1992;36:125‐30The number of CR1 on erythrocytes, as measured by monoclonal antibodies, remains undefined because of the repetitive structure of CR1 and the presence of different types of structural CR1 alleles. We studied the number of CR1 per erythrocyte using two monoclonal antibodies. E11 and 3D9, which recognize different sites on CR1. The number of binding sites was higher for E11 than for 3D9 (ratio E11/3D9: 1.9 ± 0.4, n=17); however, this ratio was not affected by CR1 numbers or alleles. Partial digestion with papain of CR1 on erythrocytes abolished the binding of 3D9. It reduced the binding of E11 to one‐third of its initial value (0.35 ± 0.03; n= 13) using cells with different CR1 numbers or alleles. By immunoblotting, a unique 75‐kDa stump of CR1 remained attached to the erythrocytes for every allele studied. Taken together, these results suggest that the number of CR1 has been over‐estimated in the past using E11 by a factor of 2, or more probably 3. However, the over‐estimation of CR1 number has been identical for erythrocytes bearing different CR1 numbers or alleles.
Antibodies against Secreted and Non‐Secreted Antigens in Mice after Infection with Live Mycobacterium tuberculosis
Authors: VERBON A. , KUIJPER S. , JANSEN H. M. , SPEELMAN P. , KOLK A. H. J. 
Published: June 2006

Mice from four different inbred strains were infected with live Mycobacterium tuberculosis and the immune response to M. tuberculosis was followed for 24 weeks, using Western blotting. Nearly all mice, irrespective of H‐2 type, reacted with the 3S‐kDa protein band. Antibodies against this secreted 38‐kDa protein were ihe first to appear, 4 weeks after infection. Thereafter the secreted 19‐kDa protein and non‐secreted antigens, such as the 65‐kDa and 33‐kDa proteins, were recognized. The immune response against the non‐secreted antigens was influenced by the mouse strain. However, the 33‐kDa protein band was recognized by all mouse strains after a second injection wilh live M. tuberculosis.The specificity of the antibodies was analysed in Western blot using sonicates of M. tuberculosis, M. kansasii, M avium. M. terrae, M. gordonae and Escherichia coli. Antibodies against the 38‐kDa and 33‐kDa protein bands seemed to be specific for M. tuberculosis, while antibodies against the 19‐kDa protein band showed limited cross‐reactivity. Antibodies against the 65‐kDa prolein were strongly cross‐reactive.These results suggest that the 38‐kDa protein is secreted in vivo and, therefore, may be available to the humoral immune system at an early stage of infection. The non‐secreted 33‐kDa protein is only recognized by all mouse strains afler prolonged contact with M, tuberculosis.
Expression of CD11b (Leu15) Antigen on CD3+, CD8+, CD16+ Peripheral Lymphocytes, Estimation of CD3+8+11b+ and CD3+4‐8‐11b‐ T‐Cell Subsets using a Single Laser Flow Cytometer
Authors: GANE P. , FAIN O. , MANSOUR I. , ROQUIN H. , ROUGER P. 
Published: June 2006

CD11b (Leu15) epitope is expressed on 20‐30% of peripheral blood lymphocytes, including CD16+ large granular lytnphocytes and CD8+ cells. This study confirms that 30% of CD8+ lymphocytes and virtually all CD16+ NK cells from healthy subjects express this determinant. In parallel, our data show that various proportions of CD3+ 4‐8‐, TCR‐δ cytotoxic T lymphoeytes and occasionally CD4+ lymphocytes subsets could also express this epitope.The CD8+ 11b+ phenotype is associated with suppression of T‐cell proliferative response and has been extensively used to characterize suppressor T lymphocytes. Since about 25% of CD8 lymphocytes are non‐T (CD3) and express the CD16 NK antigen (CD8+ 16+ 3 ‐), the expression of CD11b was also studied on CD8+ 3+ T‐cell and CD8+ 16+ NK‐cell subsets. To this end, we developed three methods using a flow cytometer equipped with a single laser and two fluorescence detectors. Results showed that T CD8+ 3+ 11b+ and NK CD8+ 16+ 11b+ lymphocytes account for 3O% and 70% of CD8+ 11b+ cells respectively. Consequently, the CD8+ 3+ 11b+ phenotype would be more specific for suppressor T lymphocytes than the total CD8+ 11b+ phenotype which includes high proportions of CD16+ NK cells.
Immune Events in Skin. I. Spontaneous Cluster Formation of Dendritic (Veiled) Cells and Lymphocytes from Skin Lymph
Authors: GALKOWSKA H. , OLSZEWSKI W. L. 
Published: June 2006

To investigate the mechanism of spontaneous attachment of afferent lymph lymphocytes to dendritic cells, cells from canine skin lymph were used. There were 3.3 ± 2.8% of veiled cells in clusters found in lymph flowing from the cannulated lymph vessel. The number of clusters forming ex vivo in the collected lymph samples increased as a function of time and was temperature dependent. Incubation of cells with proteolytic enzymes or monosaccharides did not alter cell interactions. The ability of veiled cells to bind lymphocytes was independent of divalent cations but reduced by xylocaine and retinoic acid. Among steroids only methylprednisolone showed an inhibitory effect on cluster formation, Indomethacin and acetylsalicylic acid had no blocking activity on cell binding. Also, no effect was seen after treatment with cycosporine A and azathioprine. An enhanced cluster formation after desialation with neuraminidase was observed The desialated cells were cultured in order to study their stimulatory and accessory cell functions. No enhancement of autologous mixed leucocyte reaction was seen, but a significantly higher responsiveness to a suboptimal dose of phytohaemagglutinin was observed. The N‐ase‐mediated non‐specific cell attachment could be abrogated by cell washing or treatment with EDTA or xylocaine.This study indicates that cluster formation by skin lymph veiled cells and lymphocytes is a spontaneous process which cannot be controlled by means usually effective in regulating the in vitro induced clustering of antigen‐stimulated cells.
Analysis of HLA Genotypes and Susceptibility to Insulin‐Dependent Diabetes Mellitus: HLA‐DQα Complements HLA‐DQβ
Authors: BAISCH J. M. , O'BRIEN M. E. , HOOVER M. L. , CAPRA J. D. 
Published: June 2006

It is well known that certain genes in the HLA‐D region confer increased susceptibility to insulin‐dependent diabetes mellitus (IDDM), Previous studies have documented an increased risk associated with the HLA‐DRβ chain alleles, DR3 and DR4, and the DQβ chain allele DQB1*0302 (formerly DQw8). Since DQα is also polymorphic and has been strongly implicated as the primary IDDM susceptibility locus in other races, we wanted to assess the contribution of DQα to IDDM in Caucasians, This information would enable us to define more precisely the class II association with IDDM as well as gain insight into issues of cu versus trans association of DQ heterodimers in this disease. To this end, the DQa genotype was determined for a large group of diabetic and normal Caucasian individuals who had been HLA‐DQβ and HLA‐DR typed previously. Using the polymerase chain reaction and a set of twelve oligonucleotide probes, we determined the DQα genotype of 323 patients with IDDM and 182 normal subjects.We found that certain DQα alleles are decreased in the diabetic population compared with normal subjects (i.e. DQA1*102 and 0103), while others are significantly increased in patients with IDDM (i.e. DQA 1*0301 and *0501), In addition, certain combinations of DQα alleles are associated with increased susceptibility to disease (i.e. DQA 1*0301, *0501), These results parallel our findings at the DQβ locus; however, because of the various associations between DQα and DQβ chains, the risks conferred by DQα are generally lower than those at DQβ, Moreover, our data indicate that, in Caucasians, no single DQα allele accounts for the highest degree of susceptibility to IDD M as in other races, although DQα analysis may be informative in a few cases. When done in combination, however, oligonucleotide analyses at both DQβ and DQα complement each other and provide a more complete assessment of the HLA‐associated component of disease susceptibility in IDDM