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Biomedical subjects

L Degos

Publications and source records attributed to L Degos.

At least 307 records · Page 17Linked to original sources
PubMed1977

Reactivity of anti-HLA sera against mouse lymphocytes.

The reactivity of anti-HLA hyper-immune sera was tested by the microlymphocytotoxicity technique (LCT) against a panel of mouse lymphocytes. Three levels of reactivity were observed: negative (immune sera titre 1:20 or less), weak (titre 1:40 to 1:80 with a percentage of dead cells less than 50%) or strong (titre 1:60 or more with 100% killing). Thirteen normal human sera were non-reactive. Eleven out of 60 hyper-immune sera were strongly reactive. Tests using congenic lines showed that the reactivity was controlled at the H-2 complex. One serum (CODRON) was studied in detail. When tested against a panel of strains carrying 10 different H-2 haplotypes, it reacted strongly against lymphocytes H-2d, ja, k, p and r; and did not react, or at least only weakly, against lymphocytes H-2b, f, q, s and v. Tests using mouse strains carrying the recombinant H-2 haplotypes h4, i5, i, y2, g, g2 and t1, suggested that the observed reactivity was directed against structures controlled at the K end of the H-2 complex (H-2.47?). Absorption-elution experiments with human and murine lymphocytes and platelets confirmed that the structures recognised by serum CODRON were determined at the major histocompatibility complex.

Animals↗
PubMed1977

HLA antigens in 16 families with xeroderma pigmentosum.

Xeroderma pigmentosum is an autosomal recessive disease. HLA-A and -B typing was performed on peripheral blood lymphocytes and platelets. Sixteen Tunisian families were typed with 37 patients and 108 relatives. Genetic transmission of the disease and of the HLA system seemed to be independent in this study. Comparison of HLA gene frequencies between (unrelated) parents of patients and a control population showed no difference, proving that there is no clear association in populations between deleterious XP genes and a particular HLA gene. However, an excess of identical HLA among pairs of diseased siblings would suggest that the disease is polymorphic and a form of the XP could be linked to HLA.

Blood Platelets↗
PubMed1977

Molecular defect in platelets from patients with bernard-soulier syndrome.

An IgG antibody isolated from the serum of a patient with the Bernard-Soulier syndrome induced platelet agglutination in the platelet-rich plasma of 50 normal subjects regardless of their ABO, KOa, KOb, HLA, or PlA1 types. This antibody was nonreactive with platelets from three other Bernard-Saulier syndrome patients. Indirect immunoprecipitation tests using this serum (or purified IgG) and soluble membrane antigens labeled with 125I that had been extracted from normal platelets by the nonionic detergent Nonidet P-40 gave a single radioactive peak at 150,000 MW in sodium dodecyl sulfate-polyacrylamide gel electrophoresis. These findings strongly suggest that the antigenic determinant reacting with this antibody is absent from platelets of Bernard-Soulier syndrome patients and that the deficient molecule is of 150,000 MW. The role of this molecule in subendothelial adhesion and macromolecular-mediated aggregations is discussed.

Antibodies↗
PubMed1977

Correspondence analysis of HLA gene frequency data from 124 population samples.

Correspondence analysis, a variant of principal components analysis, is used to interpret and compare gene frequencies of the HLA system for 124 samples from different populations studied in the Fifth and Sixth International Histocompatibility Workshops. The major advantage of this analysis is that populations and HLA genes are represented simultaneously with respect to the same axes in multidimensional space. This permits the visual interpretation of genetic differences between populations, the relative participation of each gene in the dispersion, and the correspondence between populations and genes. By this method a clear separation of ethnic groups in the world is obtained. Furthermore, within Europe the separation of samples from different countries is concordant with their geographical distances. The HLA system appears sufficiently polymorphic to define a population by its gene frequencies.

Asian People↗
PubMed1976

A "natural" anti-HLA-A2 antibody reacting with homozygous cells.

In the serum of a young normal male, never transfused, a cold cytotoxic IgM antibody was found reacting exclusively with A2 homozygous cells on a French panel, as shown by population and family studies. This antibody needs about two to five times more lymphocytes or platelets to be absorbed than an immune anti-A2 of the same titre. The antigen recognized by this antibody seems to be covered by the same molecule as HLA-A2, according to redistribution experiments.

Adult↗
PubMed1975

The HL-A gene structure of Twareg populations. II. The Kel Dinig.

The HL-A groups of 138 Kel Diniq Twaregs were determined by the platelet complement fixation microtechnique. Their HL-A characteristics, compared to those of Caucasoid populations, are: decrease in HL-A2, 9, W17 and W15; increase in W28, W32, HL-A7, W5, W10 and second locus blank; absence of Da25 (W30 plus W31), HL-A13, W15, W18, W27. This genetic structure is in accordance with the isolated condition of this population. The most frequent haplotypes are W28,HL-A7, common to both the Kel Diniq and the Kel Kummer Twaregs previously studied; W32,W10 and HL-A3, HL-A5, Kel Diniq only. These two populations are both isolates, with a common origin the seventeenth century, but separated as from that date. Genealogical studies have enabled the haplotype W28,HL-A7 to be attributed to the two brothers who founded the populations in the seventeenth century. A comparison of these two populations constitutes a model for the study of genetic drift and the founder effect.

Complement Fixation Tests↗
PubMed1975

Combined analysis of three studies of patients with Burkitt's lymphoma.

Data from the three preceding studies on the possible relationship of HL-A type with Burkitt's lymphoma were combined to see whether any trends in the data, not significant in the individal studies, would show significance when the three groups were combined. A statistical method for combining data from different studies is developed. Although in this analysis even the combined data failed to show any significant association of HL-A type with disease, it is suggested that the statistical methods used will be helpful in analysing other sets of data where it seems desirable to combine information from several studies.

Burkitt Lymphoma↗
PubMed1975

HL-A phenotyping in an Indonesian population.

The frequencies of 30 HL-A antigens were studied in an Indonesian population of 95 individuals from the city of Jakarta. The antigens HL-A9, or more precisely W24, and HL-A11 (first series) and W15 (second series) occurred with high frequencies, whereas HL-A8, W14 and W22 were completely absent. These results are consistent with previous reports of HL-A typing in South East Asian populations.

Complement Fixation Tests↗
PubMed1975

A molecular defect in thrombasthenic platelets.

An IgG antibody found in the serum of a thrombasthenic patient reacted in complement fixation with platelets from 350 normal individuals but was nonreactive with platelets from eight other thrombasthenic patients. ADP-induced aggregation of normal platelets was inhibited by the patient's antibody. Family studies using the quantitative complement fixation test showed that healthy heterozygotes were easily distinguishable from normal or thrombasthenic individuals since their platelets had an intermediate amount of the reactive antigen. Indirect immunoprecipitation tests using this serum and soluble membrane antigens labeled with iodine-125 that had been extracted from normal platelets by the detergent Nonidet P-40 gave a single radioactive peak at 120,000 mol wt in sodium dodecyl sulfate polyacrylamide gel electrophoresis. A similar estimate of the molecular weight was obtained from Sephadex G-200 filtration of the soluble antigens extracted from normal platelets by spontaneous release or chaotropic agents and tested in complement fixation with the patient's serum. These findings strongly suggest that the molecule recognized by this antibody is absent or structurally modified in thrombasthenia cases and that it may be involved in platelet aggregation.

Adenosine Diphosphate↗
PubMed1975

Formal genetics of the HL-A region.

The extreme polymorphism of the HL-A system is due to the presence of two (SD1, SD2) and perhaps three linked polyallelic genes. The distinction of "bridging antibodies" (reacting with several HL-A specificities recognizing separate sites on the HL-A molecule) from the main HL-A determinant as it is demonstrated by absorption/inhibition experiments increases this complexity. The HL-A linkage group is composed of other systems: LD1, LD2, PGM3, ADA (?), P, ME1, IPO-B and possibly a "hay fever gene". No gametic or zygotic selection was found in spite of the presence of HL-A antigens on spermatozoa. Mixed lymphocyte reaction (MLR) is principally governed by LD genes. The main (LD2) gene is probably situated outside the interval SD1, SD2, near SD2. Other LD genes (LD1 inside the interval SD1-SD2 and LD3) are suspected. The presence of an immune response gene (Ir) has not yet been demonstrated although several diseases associated with specific SD2 antigens are known. These different genes (SD1, SD2, LD1, LD2, LD3 and Ir) probably form a functional unit in the allo-immunozation.

Alleles↗