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R Oriol

Publications and source records attributed to R Oriol.

At least 109 records · Page 6Linked to original sources
PubMed1992

Serological and chemical specificities of twelve monoclonal anti-Lea and anti-Leb antibodies.

The serological specificities of twelve hybridomas were compared as to their chemical reactivity as determined using direct binding to synthetic carbohydrate structures. All anti-Lea cross-react with type-1-precursor structures and three different variants of anti-Lea could be defined by their binding to type-3-precursor chains, sialylated compounds and the monosaccharide D-galactose. Three major reactivity patterns were also identified among anti-Leb reagents. Anti-LebL cross-react with Lea and do not significantly bind to H-related structures. Anti-LebH,L had both anti-LebL-like activity (cross-reaction with Lea) and anti-LebH-like activity (cross-reaction with H). Finally, anti-LebH cross-reacts strongly with H compounds and do not bind to Lea. The binding pattern of anti-LebL suggests that these antibodies have lower affinity for ALeb and BLeb pentasaccharides than anti-LebH. All these specificities are not absolute, but rather are expressed as members of a quantitative progressive varying series, suggesting the existence of a whole range of antibody specificities gradually changing from Lea----Lea,b----LebL----LebH,L----LebH. The results suggest that anti-LebL will always cross-react with Lea and that anti-LebH will always cross-react with H related structures. However, under certain well-defined conditions these cross-reactions may not be apparent and antibodies might behave as specific anti-Lea or anti-Leb in certain tests.

Antibodies, Monoclonal↗
PubMed1992

Genetic regulation of the expression of ABH and Lewis antigens in tissues.

Sequential appearance of ABH antigens in different animal species shows a progression from tissues of endodermal to ectodermal and finally mesodermal origin, human erythrocytes being the last cells to acquire these antigens. In view of this, ABH antigens should be called tissue or histo-blood group antigens rather than blood group antigens. In addition to the glycosyltransferases encoded by the ABO genes, several alpha-2, alpha-3 and alpha-4-fucosyltransferases are needed to account for the known ABH histo-blood group antigens. The genetic polymorphism of the genes encoding each of these enzymes defines inter-individual differences. In addition, in the same individual various tissues express these antigens in a different way. For each adult epithelial tissue, antigenic expression is related to cell maturation from germinal layer to surface epithelium. Differential expression is also found at various embryonal stages of the same cells. Examples of these phenomena are presented in an effort to gain further insight into the genetic regulation of the expression of these complex oligosaccharide molecules.

ABO Blood-Group System↗
PubMed1991

HgCl2-induced perturbation of the T cell network in experimental allergic encephalomyelitis. I. In vitro characterization of T cells involved.

Mercuric chloride (HgCl2) induces in Lewis (LEW) rats a non-antigen-specific immunosuppression and is able to down-modulate experimental allergic encephalomyelitis in about 70% of the rats. The aim of the present study was to determine the frequencies of lymph node cells involved in the proliferative response to myelin basic protein in rats injected with HgCl2 and immunized with myelin by using limiting dilution analysis (LDA). Highly frequent CD8+ T suppressor cells and at least 10-fold less frequent protein basic-specific T helper cells were detected in these rats. A third cell type allowing the proliferative response of Th cells in spite of Ts cells was also demonstrated. These cells, which could act as contrasuppressor cells, were CD4+ and adhered to Vicia villosa lectin; their frequency was in the same range as that of T helper cells. These data illustrate the potential role of different levels of T cell immunoregulatory activity in autoimmunity and the major interest of LDA in their analysis.

Animals↗
PubMed1991

HgCl2-induced perturbation of the T cell network in experimental allergic encephalomyelitis. II. In vivo demonstration of the role of T suppressor and contrasuppressor cells.

In the companion paper (J. Rossert et al., Cell. Immunol. 137, 1991), we showed by using limiting dilution analysis that Lewis (LEW) rats injected with HgCl2 and immunized with myelin (LEWHg/MYE) exhibit anti-basic protein CD4+ T helper cells (Th), at least 10-fold more frequent CD8+ T suppressor cells (Ts), and T contrasuppressor cells (Tcs). These Tcs cells were shown to be CD4+ T cells adhering to Vicia villosa (VV) lectin and allowed Th cells to proliferate despite the presence of Ts cells. The CD8+ Ts cells might be responsible for the protection from experimental allergic encephalomyelitis (EAE) observed in about 70% of LEW rats injected with HgCl2. The concomitant presence of CD4+ Tcs cells might explain that 30% of the rats escaped this protection. The aim of this work is to demonstrate in vivo the roles of CD8+ Ts cells and Tcs cells in mercury-induced protection from EAE. It will be shown that LEWHg/MYE rats depleted of CD8+ cells as well as LEWHg/MYE rats transferred with VV lectin-adherent Tcs cells develop EAE. These data demonstrate that CD8+ Ts cells are responsible for HgCl2-induced protection and that Tcs cells are involved in the control of Ts cells in vivo.

Animals↗
PubMed1991

The human chromosome 19 linkage group FUT1 (H), FUT2 (SE), LE, LU, PEPD, C3, APOC2, D19S7 and D19S9.

Families segregating for deficiency of the H alpha-2-L-fucosyltransferase, FUT1, have been investigated for linkage between FUT1 and other markers on chromosome 19. The results provide evidence for close linkage between FUT1 and FUT2 and for looser linkage between FUT1 and APOC2 and between FUT1 and D19S7. Pairwise linkage data are also reported between other markers investigated.

Blood Grouping and Crossmatching↗
PubMed1991

Chromosome 11q localization of one of the three expected genes for the human alpha-3-fucosyltransferases, by somatic hybridization.

Seventy-one human x mouse hybrid cell lines were used to map the locus of a human alpha-3-fucosyltransferase to 11q. The enzyme transfers fucose onto H type 2 more efficiently than onto sialyl-N-acetyllactosamine, suggesting that it is the myeloid type of alpha-3-fucosyltransferase (Mollicone et al., 1990), which makes the 3-fucosyllactosamine epitope on polymorphonuclear cells and monocytes. This epitope is also known as CD15 (Tetteroo et al., 1987).

Animals↗
PubMed1990

F11C antigen: a membrane marker able to distinguish two regressive and progressive variants from a rat colon adenocarcinoma.

Cell variants that differ in their tumorigenicity and immunogenicity have been isolated from a BDIX rat colon adenocarcinoma cell line, DHD/K12. One variant, PRO, and the clones derived from it, are poorly immunogenic and induce progressive and metastatic tumors; the other one, REG, and its clones, are highly immunogenic and induce regressive tumors. When looking for a membrane marker distinguishing between PRO and REG lines, we obtained monoclonal hybridomas by immunizing BALB/c mice with PROb or REGb cell clones. Hybridoma F11C, producing an IgM monoclonal antibody (MAb) was able to distinguish between the cell variants on membrane immunofluorescence. All REGb cells strongly express F11C membrane antigen. On PROb cells, F11C antigen expression is weak, as demonstrated by cytofluorimetric analysis, and limited to a fraction of the cell population. The F11C membrane antigen is highly specific for the DHD/K12 cell line and the variants derived from it, but is not expressed on cells dissociated from the DHD transplanted tumor, from which DHD/K12 was established, suggesting that F11C antigen emerged during cell culture. Fluorescence absorption on synthetic oligosaccharides demonstrated that F11C antibody cross-reacts with A type 3, A type 4 and A type 5 chain blood group tetrasaccharides.

Adenocarcinoma↗
PubMed1990

Acceptor specificity and tissue distribution of three human alpha-3-fucosyltransferases.

Based on the capacity to transfer alpha-L-fucose onto type-1 and type-2 synthetic blood group H and sialylated acceptors, a comparison of the alpha-3-fucosyltransferase activities of different human tissues is shown. Three distinct acceptor specificity patterns are described: (I) myeloid alpha-3-fucosyltransferase pattern, in which leukocytes and brain enzymes transfer fucose actively onto H type-2 acceptor and poorly onto sialylated N-acetyllactosamine: (II) plasma alpha-3-fucosyltransferase (EC 2.4.1.152), in which plasma and hepatocyte enzymes transfer, in addition, onto the sialylated N-acetyllactosamine; (III) Lewis alpha-3 4-fucosyltransferase (EC 2.4.1.65), in which gall-bladder kidney and milk enzymes transfer, in addition, onto type-1 acceptors. The small amount (less than 10%) of alpha-3-fucosyltransferase activity found in the plasma of an alpha-3-fucosyltransferase-deficient individual had a myeloid-type acceptor pattern, suggesting that this small proportion of the plasma enzyme is derived from leukocytes. In addition to the three acceptor specificity patterns, these enzyme activities can be differentiated by their optimum pH: 8.0-8.7 for the enzymes from myeloid cells and brain. 7.2-8.0 for liver enzymes and 6.0-7.2 for gallbladder enzymes. Milk samples had two alpha-3-fucosyltransferase activities, the Lewis or alpha-3/4-fucosyltransferase under control of the Lewis gene and an alpha-3-fucosyltransferase with plasma acceptor pattern which was independent of the control of the Lewis gene. The apparent affinity for GDP-fucose of the myeloid-like enzyme was weaker than those of the plasma and Lewis-like enzymes. The apparent affinities for H type 2 and sialylated N-acetyllactosamine were stronger for exocrine secretions as compared to the plasma and myeloid enzymes. The plasma type of alpha-3-fucosyltransferase activity was more sensitive to N-ethylmaleimide and heat inactivation than the samples with myeloid-like alpha-3-fucosyltransferase activity.

Brain↗
PubMed1990

Differential susceptibility to experimental allergic encephalomyelitis (EAE) in genetically defined A+ and A- rabbits.

Only one out of 57 A-/A- rabbits immunized with rat or guinea-pig myelin developed clinical signs suggestive of EAE. On the contrary, clinical signs of acute or chronic EAE were found in two thirds of the 102 A+/A+ and A+/A- rabbits immunized in the same way. About one third of the diseased animals had reversible acute EAE, another third died paralysed and the last third developed chronic progressive or relapsing EAE. Incidence and severity of EAE symptoms were positively correlated with age and no significant difference was observed between males and females. Cellular and humoral anti-myelin responses were stronger in A+ than in A- rabbits. Anti-A antibodies, on the contrary, were only detected in A- rabbits. The A+ rabbits did not make Anti-A at any time. Anti-A antibodies increased early, in A- rabbits, after immunization with myelin (11-30 days) and were later replaced by a low, but specific, anti-myelin response (60-90 days). The gene responsible for the susceptibility to EAE is autosomal and dominant over resistance. This gene must be closely linked to the A locus or might be the A gene itself. The low susceptibility of A- rabbits to the disease could be, in this last case, a consequence of the competition between the early anti-A and the normal anti-myelin immune responses, both induced by the injection of myelin.

ABO Blood-Group System↗
PubMed1989

Cellular expression of H and B antigens in the rat olfactory system during development.

Developmental expression of H and B antigens in the rat olfactory system was studied from the embryonic day 14 up to the postnatal day 30. The H antigen was detected in the olfactory and vomeronasal epithelia as early as fetal day 14, whereas the B antigen first appeared 2 days later. The anti-H reagent reacted strongly with sensory receptors and weakly with supporting cells in both epithelia, whereas the anti-B reagent was specific for olfactory receptors. In the main olfactory epithelium, the H antigen was expressed from fetal day 19 by most of the receptor cells, whereas the B determinant was expressed from fetal day 16 to postnatal day 3 by only a few neuroreceptors mostly located near the epithelial surface. After the postnatal day 3, B positive neurons increased in number from the periphery toward the deeper mucosal layers and they were distributed over 3/4 of the epithelial thickness in 15- and 30-day-old rats. In the main olfactory bulb, a widespread glomerular B staining with variable binding intensity between adjacent glomeruli was already observed at birth. The vomeronasal receptor cells and their axon terminals in the accessory olfactory bulb exhibited a comparable developmental expression of the B antigen. Results suggest that the B antigen could be regarded as a marker of neuronal maturation of both the olfactory and vomeronasal receptor cells; moreover, its first appearance in the receptor cells might be temporally related to the formation of synapses between receptor axons and deutoneurons in the bulb.

ABO Blood-Group System↗
PubMed1989

Appearance of B and H blood group antigens in the developing cochlear hair cells.

The presence of human blood-group antigens was analyzed in the rat cochlea during its postnatal development, using anti-A, anti-B and anti-H antibodies. At no stage was reactivity with anti-A antibody observed. With the anti-H antibody, a strong reactivity was observed from 1 to 9 days after birth within hair cells and some other surface epithelial cells of the cochlear duct. After postnatal day 9, only a faint reactivity persisted in a few non-sensory cells. With the anti-B antibody, only hair cells were selectively labeled. At early stages (postnatal day 1 and 3), the reactivity was intense and observed both around the cell surface and within the supranuclear region of cytoplasm. Later on, the reactivity decreased; it was limited at postnatal day 9 to a reactive spot below the cuticular plate. Results are compared with a preliminary finding describing the first appearance of B and H antigens in the organ of Corti at a prenatal stage, and with data concerning other sensory and neural structures. The appearance and progressive disappearance of B and H antigens on sensory and non-sensory cells can be correlated with significant events in the development of the cochlea. The transient expression of B and H antigens in cochlear sensory cells may correspond to developmental changes in their surface glycoconjugates.

ABO Blood-Group System↗
PubMed1989

Expression of ABH, Lewis and related tissue antigens in the human thymus.

Expression of ABH, Lewis and related antigens was studied in the thymus of children of known ABO, Lewis and secretor status using a panel of specific reagents. ABH and Lewis antigens partly under control of the secretor status were expressed on the Hassals' bodies and a large fraction of the medullary epithelial cells. The sialyl-Lea antigen was only present on some Hassals' bodies of Lewis-positive individuals. ABH but not Lewis antigens were also present on cortical epithelial cells but this was independent of the secretor status. The X, sialyl-X and Y antigens were only expressed on Hassals' bodies irrespective of the ABO, Lewis or secretor phenotype. Furthermore, the anti-X and sialyl-X antibodies labelled a subset of leucocytes of all the individuals tested. These results show that the genetic control of the expression of ABH and Lewis glycosidic tissue alloantigens in the thymus is different on cortical and medullary epithelial cells and stress the heterogeneity of the thymus epithelial cells.

ABO Blood-Group System↗
PubMed1989

The role of ABO blood group compatibility in heart transplantation between closely related animal species. An experimental study using the vervet monkey to baboon cardiac xenograft model.

The role of ABO blood group compatibility on graft survival when transplantation is performed between closely related animal species is uncertain. Heart transplants (in the neck) were performed between donor vervet monkeys and recipient baboons; no immunosuppressive therapy was given. Survival in ABO-compatible pairs (group 1, n = 9) was for a mean of 10.3 (+/- 5.2) days, which was not significantly different from that in ABO-incompatible pairs (group 2, n = 9: mean survival 7.3 +/- 5.6 days). In group 2, however, three hearts were rejected hyperacutely within 60 minutes, whereas in group 1 only one heart was rejected within 24 hours (not significant). Preformed anti-vervet monkey antibody was present in only one of 18 baboons, but developed in eight others. ABO-specific antibodies were present in all nine group 2 baboons and increased in titer in six cases. Histopathologic features of vascular (humoral) rejection, sometimes associated with cellular infiltration, were seen in a majority of hearts in both groups. Though the number of animals in this study was small, ABO-incompatibility would not appear to be a major factor in cardiac xenograft survival when transplantation is performed between closely related primate species, though early hyperacute rejection would seem more likely to occur when blood group incompatibility is present.

ABO Blood-Group System↗
PubMed1988

Immunochemical characterization of mucins. Polypeptide (M1) and polysaccharide (A and Leb) antigens.

Seven monoclonal antibodies (MAbs) reacting with high-molecular-mass components (greater than 20,000 kDa) isolated from an ovarian mucinous cyst of an A Le(a-b+) patient are described. By the use of immunoradiometric methods, these MAbs characterized seven different epitopes associated with components having a density of 1.45 g/ml by CsCl-density-gradient ultracentrifugation, like mucins. Two MAbs reacted with A and Lewis blood-group antigens respectively (polysaccharide epitopes). The five other MAbs characterized five M1 epitopes (called a, b, c, d and e), mainly associated with components of more than 20,000 kDa and 2000 kDa. They were completely destroyed by papain and 2-mercaptoethanol treatment (polypeptide epitopes). Moreover, timed trypsin digestion of native mucin resulted in a progressive loss of M1 activity and degraded these mucins into smaller M1-positive fragments. The a and c epitopes were partially degraded from relatively high-molecular-mass fragments (2000 kDa to 500 kDa) into a 100 kDa fragment. The b and d epitopes were completely degraded into smaller fragments ranging from 100 kDa to 40 kDa. The e epitope was completely destroyed by trypsin. These different pathways of M1 antigen degradation suggest the occurrence of different epitopes located in separate regions of the mucin molecules.

Antibodies, Monoclonal↗
PubMed1988

Ectopic expression of the Y (Ley) antigen defined by monoclonal antibody 12-4LE in distal colonic adenocarcinomas.

Monoclonal antibody (MAb) 12-4LE reacts specifically with the alpha Fuc(1-2) beta Gal(1-4) [alpha Fuc(1-3)]GlcNAc-R synthetic oligosaccharide and consequently characterizes the Y (Ley) antigen. In normal individuals, this MAb reacts more strongly on samples from blood group O persons, indicating that the Y structure is better recognized when terminal A or B sugars are not added to the Y structure. In fetal and normal adult gastrointestinal tract, this antibody reacts with the epithelium of stomach, small intestine and proximal colon, but not of distal colon. In the adult, cells from the surface epithelium of the gastric, small intestinal and cecal mucosae express the Y antigen according to the secretor phenotype of each individual, thus characterizing the so-called "upward differentiation" pattern. In contrast, mucus cells of the pylorus and duodenal Brünner glands, as well as Paneth cells, always express the Y antigen irrespective of secretor phenotype, thereby characterizing the so-called "downward differentiation" pattern. Proximal fetal colonic mucosa has the same genetic control as the downward differentiation pattern of the adult. Distal fetal colonic mucosa is negative with anti-Y, as in the adult. Y antigen was not expressed in hyperplastic (10 cases), juvenile (5 cases) or adenomatous (43 cases) polyps, except for some spreading villous adenomas in which rare Y-positive foci could be observed but which were not specifically associated with dysplastic glands. Polyps from familiar polyposis did not express this antigen. In adenocarcinomas, the Y antigen was expressed in 41/45 (91%) of distal tumors and 15/35 (43%) of cecal tumors, independently of ABO phenotype. The ectopic expression of this Y antigen on distal colon adenocarcinomas may be a useful tool in the detection of distal colonic carcinomas.

ABO Blood-Group System↗
PubMed1988

Effect of HgCl2 on experimental allergic encephalomyelitis in Lewis rats. HgCl2-induced down-modulation of the disease.

HgCl2 induces autoimmunity in Brown-Norway rats and immunosuppression in Lewis rats. In the latter rats, HgCl2 triggers the proliferation of T suppressor/cytotoxic (OX8+) cells which actively suppress T cell functions. This led us to study the effect of HgCl2 on experimental allergic encephalomyelitis (EAE), a T cell-mediated autoimmune disease obtained following immunization with basic protein (BP). It will be shown that HgCl2 attenuates or even prevents clinical manifestations of EAE and inhibits both the proliferative response of T cells to BP and the anti-BP antibody response. This immunosuppression was not due to a defect at the T helper cell or antigen-processing cell level but to the emergence of T suppressor cells.

Animals↗
PubMed1988

Developmental modifications of sheep kidney antigens.

We have used monoclonal antibodies to study the changes in the expression of four kidney antigens during organogenesis in the sheep. Two of these antibodies, EE24.6 and EJ30.1, label intensely only the adult kidney, whereas the other two, EK17.1 and EJ15.1, bind to the extracellular matrix of the embryonic kidney. For EJ15.1, the staining of the extracellular matrix decreases temporarily during the second half of intrauterine life, a period during which a light staining appears in the mesangium. For the other, EK17.1, the extracellular matrix staining in the stroma gradually decreases as the embryo grows, while staining of the mesangium and the arterial intima becomes evident. With EK17.1, fibronectin is identified in the extracellular matrix of the embryonic kidney and intracellularly in the mesangial cells after these cells have colonized the glomerulus. The mesonephros staining seems to be the same as that of the metanephros. In the adult, extraglomerular vascular endothelial cells bind EK17.1, whereas intraglomerular endothelial cells do not express fibronectin, which suggests a functional difference between endothelial cells in these two localizations.

Animals↗