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V Lepage

Publications and source records attributed to V Lepage.

85 records · Page 5Linked to original sources
PubMed1978

A haplotype study of HLA complex with special reference to the HLA-DR series and to Bf. C2 and glyoxalase I polymorphisms.

Fifty-three French families were typed for alleles at seven loci of the HLA complex (HLA-A, -B, -C, -DR, -Bf, -C2 and -GLO) and 212 haplotypes were demonstrated. Eleven recombinations were observed (two A/B, two A/C, two B/Bf, one Bf/D and four D/GLO). The linkage disequilibrium was calculated not only between two alleles (delta) but between three, four...seven alleles (D). In order to compare the intensity of D values in the various haplotypes, the influence of the differences in gene frequencies was eliminated by the introduction of the standardized Ds (Ds = D/D max). The number of haplotypes in disequilibrium is relatively limited since most of the significant Ds involved about 17 haplotypes. For some haplotypes, the disequilibrium covered the whole distance from A to GLO but the stronger disequilibrium concerns the C to Bf or C to DR segment. Three hypotheses (isolation, admixture of population and selection) concerning the formation and maintenance of the disequilibria are discussed.

Epitopes↗
PubMed1977

[The Ly-Li system, a new locus of the HLA complex].

Antibodies raised through immunization of volunteers not differing for serologically defined HLA-A, B and C antigens enabled us to define since 1975 a new antigenic system controlled by the HLA complex. These new allo-antigens, designated Ly-Li, are expressed on B lymphocytes but are absent from T lymphocytes, platelets, erythrocytes and fibroblasts. Multiple alleles belong to the Ly-Li differentiation antigen system. The gene frequencies of three alleles thus far detected are 0.1558 for Li2; 0.1867 for Li3 and 0.122 for Li4. Like in the serologically defined HLA antigen systems, "inclusions" were observed also in Ly-Li system, suggesting the existence of private and public specificities. Among 48 families, 23 were informative in showing that the Ly-Li locus segregated with the HLA complex. Data on three families with recombinant haplotypes between HLA-B and D, and between Bf and HLA-D, indicated that the Ly-Li locus was near HLA-D (possibly identical with HLA-D). Anti-Ly-Li antibodies inhibited cellular proliferation in mixed leucocyte culture (MLC) primarily when directed against the antigens of stimulator cells. There was a good correlation between Ly-Li and HLA-D alleles, particularly between Li2 and DW5 (r = 0.70). Usually, HLA-D specificities were "included" in the related Ly-Li specificities, but not vice-versa. In contrast, there was a higher correlation between Ly-Li specificities and those detected by the PLT (primed lymphocyte test). The Ly-Li system seems to be of great importance for the functional characterization of lymphocyte subpopulations, for the selection of the best donor in organ transplantation, and for the investigation of susceptibility genes in diseases associated with HLA-D.

Alleles↗
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↗
PubMedDate not supplied

European genetic study on rheumatoid arthritis: is there a linkage of the interleukin-1 (IL-1), IL-10 or IL-4 genes to RA?

UNLABELLED: The genetic predisposition for rheumatoid arthritis (RA) is only partly explained by the HLA locus and most genetic factors involved in the susceptibility (and/or severity) of the disease await further identification. The first European genome scan in RA families provided suggestive evidence for linkage with a region (3.1/3q13) on chromosome 3, but many other potential RA susceptibility genes have yet to be analysed. AIMS: To perform a linkage analysis with microsatellite markers located in the vicinity of the interleukin-1 (IL-1) gene superfamily, the IL-10 gene and the IL-4 gene cluster which might be considered putative candidate loci for RA. METHODS: 107 Caucasoid European RA sibpairs from 90 nuclear families were genotyped for markers flanking the genes for the IL-1 superfamily, IL-10 and the IL-4 gene cluster. Linkage analysis based on the identity by descent (IBD) in affected siblings was analysed with the program SIBPALNA. Affected sibpairs were stratified according to the identity by state (IBS) for three markers in the HLA region (DRB1 oligotyping, D6S276 and TNFa microsatellites) and to the presence/absence of erosive disease on X-ray examination. RESULTS: Analysis of the whole family set showed an excess of allele sharing for markers of the IL-1 gene cluster (IBD 60%; P = 0.012) but not for IL-10 or IL-4. After stratification, the evidence of linkage to IL-1 was restricted to HLA concordant sibpairs (n = 32; IBD 70%; P = 0.006). Some evidence of linkage to IL-10 was also observed in HLA concordant sibpairs (IBD 66%; P = 0.03) and in sibpairs with erosive disease (n = 61; IBD 62%; P = 0.02). CONCLUSIONS: We found suggestive evidence of linkage of RA to the IL-1 locus. The increased linkage to IL-1 and IL-10 in HLA-identical sibs suggests a possible interaction between these cytokines and the HLA loci. Moreover IL-10 could interact with HLA factors in predisposing to erosive disease. These results need to be tested in additional families for consistency and replication.

Arthritis, Rheumatoid↗