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Biomedical subjects

J P Cartron

Publications and source records attributed to J P Cartron.

At least 19 recordsLinked to original sources
PubMed1979

Galactosyltransferase and membrane glycoprotein abnormality in human platelets from Tn-syndrome donors.

Early studies on the analysis of membranes isolated from the erythrocytes of Tn-patients by SDS-polyacrylamide gel electrophoresis (SDS-PAGE) revealed a severe reduction in the staining capacity of glycophorin with the periodate-Schiff (PAS) reaction. A low sialic acid and galactose (Gal) content of the polyagglutinable red cells was confirmed while it was reported that the abnormal red cells of Tn-patients contained little or no UDPGal: GalNAc-beta-3-D-galactosyltransferase (T-transferase) activity. The glycoprotein (GP) abnormality in Tn-erythrocytes appeared to be due to incomplete synthesis of the alkali-labile oligosaccharide chaims of glycophorin. We now report studies on the membrane GP composition and the T-transferase activity of platelets isolated from there Tn-syndrome patients whose red cell membranes contain GP abnormalities which are typical of those found in this rare clinical condition.

Blood Group Antigens↗
PubMed1979

[K-Lymphocyte cytotoxicity: role of human blood group ABO, rhesus and P alloantibodies].

Using human erythrocytes of known antigenic density, sensitized by ABO and Rhesus (D) alloantibodies, it is shown that K cell cytotoxicity mediated by peripheral blood lymphocytes is directly correlated with the number of IgG molecules specifically bound to the target cell surface. The lytic sensitivity of P1k but not P2 or p erythrocytes coated with anti-Tja (anti-P + P1 + Pk) antibodies, demonstrates that effector K cells are mainly triggered through the IgG ANTI-Pk component of such sera.

ABO Blood-Group System↗
PubMed1979

Human IgE response to the administration of blood components. II. Repeated gammaglobulin injections.

43 adults from a renal dialysis unit staff have received regularly spaced gamma-globulin administrations for hepatitis B prophylaxis. Several blood samples were collected over a prolonged period of time (160 days). Following gamma-globulin administration, anti-immunoglobulin antibodies of the IgE class were detected in 80% of this population, a fortnight after the first injection using serum absorptions on polymerized gamma-globulins or a specific inverse RAST method. The reactivity pattern of these IgE anti-immunoglobulin antibodies was similar to that observed for the anti-immunoglobulin antibodies with "limited specificity" detected by passive hemagglutination, in that they reacted with only one of the immunoglobulins of the panel used for their detection. A decrease of the overall IgE levels was observed in 62% of the subjects for a prolonged period of time following gamma-globulin administration. This suggests a feedback regulation mechanism for the reagin production in man, as it has already been observed in animals. A high incidence of anti-immunoglobulin antibodies of various classes was observed in this study. However, only a small number (4/43) of adverse reactions appeared following gamma-globulin administration. For some of these subjects, the presence of specific IgE anti-immunoglobulin, detected by the inverse-RAST technique, suggests a possible role of such antibodies in some intolerance reactions to gamma-globulin administration.

Absorption↗
PubMed1979

Probable biosynthetic pathway for the synthesis of the B antigen for Bh variants.

Red cells and serum from two Bh variants (B+H-cells) have been investigated for B and H blood group glycosyltransferases. The H enzyme could not be detected using either type 1 or type 2 chain acceptors. The B enzyme was present in normal amount when 2'-fucosyllactose was used as substrate, neither 6'-fucosyllactose nor 6'-fucosyllactosamine could act as acceptors for the B enzyme. Upon treatment of the Bh red cells by the B-degrading enzyme from Trichomonas foetus the B antigen was destroyed while H determinants were uncovered (B-H + cells). The cells thus treated could be further converted into A&H-red cells by the action of the A transferase from human blood group A serum. Previous treatment of the B-H + cells by the H-degrading enzyme from T. foetus, however, led to B-/-erythrocytes and prevented their conversion into A red blood cells by the A enzyme. The results clearly demonstrate that, as found in normal B individuals, the B antigen from Bh cells is built up from the H precursor and provide additional evidence that H is not a completely silent gene in Bh individuals.

ABO Blood-Group System↗
PubMed1979

Induction of Tk polyagglutination by Bacteroides fragilis culture supernatants. Associated modifications of A B H and I i antigens.

Tk transformed red blood cells were obtained in vitro by treatment with supernatants from cultures of three different Bacteroides fragilis strains. The reactions of these cells with AB sera show that Tk is different from other known types of polyagglutination. Beside the already known modifications of A B H antigens, we found that Tk activated cells have an important modification of I and i antigens: both are reduced, and can even be completely destroyed.

ABO Blood-Group System↗
PubMed1979

Localization of blood-group A and I antigenic sites on inside-out and rightside-out human erythrocyte membrane vesicles.

Investigations of the fixation of 125I-labelled anti-A and anti-I antibodies onto rightside-out and inside-out membrane vesicles prepared from human A1 and OI erythrocytes, respectively, showed that both antibodies were bound to the rightside-out vesicles, giving clear evidence that blood group A and I antigenic sites are exclusively localized on the external surface of the membrane.

ABO Blood-Group System↗
PubMed1978

[A family with an "Hm" phenotype transmitted over 3 generations].

Hm phenotype represents a dissociation between a normal salivary expression of H substance and a very weakened expression of the antigen on red blood cells. Genetic analysis of the reported family reveals a dominant inheritance: Some members (Marie K..., Francette, Carmen) present a phenotype marked by a normal H enzyme but a deficient H antigen in erythrocyte membrane. Others Alice, Mathilde) have no expression of A1 antigen due to H substrate deficiency. H substance in salivary secretion is normal. In the other branch of this pedigree without consanguinity, Herbert presents an H substance deficiency, though quite different, as A1 antigen is expressed. In this family, Hm phenotype can be explained, without resorting to a Zm allele, by the expression of an exceptional allele at the H locus (like Am is an ABO allele). This hypothesis supports the possible polymorphism of H locus.

ABO Blood-Group System↗
PubMed1977

Antigen site distribution among weak A' red cell populations. A study of A3, Ax and Aend variants.

The distribution of the A receptors was studied among 'agglutinated' and 'free' populations of A variant RBC (A3, AX, Aend) known to be either partially or weakly agglutinated by human anti-A reagents. Following separation of the red cell populations and disaggregation of the clumps by mild treatment with soluble blood group substances, it was shown after appropriate controls, that among A3 ARBC, the 'agglutinated' RBC have at least five times as 'free' RBC, these latter however being strongly A positive. The differences between the A antigenic content of the AX RBC were less pronounced. The most striking result was obtained with the Aend RBC, where two populations are clearly demonstrated; the first, including 5-10 per cent of the RBC, strongly agglutinates with anti-A and contains erythrocytes of high antigenic content (140,000 A receptors per cell). The second, including the majority of RBC could not be differentiated from the control O RBC. A wide heterogeneity of antibody binding capacity of the various populations of A3, AX and Aend red cells, was also demonstrated following ultrastructural examination by immunoelectron microscopy with peroxidase-conjugated antibodies. Such study reveals furthermore an heterogeneity of labelling from one cell to another in the same population of red blood cells. Comparison of 'week A' RBC and O RBC enzymatically converted into A RBC, demonstrates a similar pattern of reactivity between these cells, and supports the general relationship between antigen site density and red cell agglutination. It is concluded that the typical pattern of agglutinability of A3 and AX RBC arises both from their heterogeneous antigenic content and from the occurrence of an antigenic threshold below which red cells become non-agglutinable. The typical mixed-field agglutination pattern of Aend RBC merely reflects the occurrence of a probably true dual population of RBC. Finally, the mechanisms of inheritance of such well-known Mendelian characters, enabling the production of highly heterogeneous blood cell populations in the same individual, remains to be elucidated.

ABO Blood-Group System↗