PubMed Health⌕ Search

Biomedical subjects

L Contu

Publications and source records attributed to L Contu.

At least 91 records · Page 5Linked to original sources
PubMed1979

Role of Ia-like products of the main histocompatibility complex in conditioning skin allograft survival in man.

This report correlates the survival time of 93 intrafamilial skin allografts performed under conditions of main histocompatibility complex (HLA) haploidentity with donor-recipient compatibility for products of the HLA-A, -B, -C, and -DR, as well as C3 proactivator, Glyoxalase I, and P loci located on the human 6th chromosome. Incompatibilities for HLA-A and -B (and to a lesser extent for HLA-C) and(or) for HLA-DR products exerted a strong influence upon the fate of skin allografts. When HLA-A and -B were considered alone, the most compatible group of grafts had a mean survival time of 15.8 d, as compared with 11.3 d for the most incompatible transplants. HLA-DR compatibility alone was associated with a mean survival time of 15.3 d, whereas HLA-DR-incompatible grafts had a mean survival time of 11.5 d. Incompatibilities for C3 proactivator, Glyoxalase I, and P did not have a significant effect upon graft survival. There was no evidence of an association between donor-recipient incompatibility at HLA-A, -B, or -C or at HLA-DR; such incompatibilities occurred independently of each other, in spite of the state of linkage disequilibrium known to exist between HLA-B and -DR. Incompatibilities for HLA-A, -B, and for HLA-DR exerted a potent additive effect upon graft survival. Skin grafts bearing one, two, or three incompatibilities had a mean survival time of 16.2, 13.7, and 10.7 d, respectively (P <0.0005).The results point to the important role played by the Ia-like products of the HLA complex (HLA-DR) in conditioning skin allograft survival in man. This consideration may be of direct relevance to the potential clinical usefulness of in vitro serological techniques for the detection of donor-recipient compatibility for HLA-DR.

Female↗
PubMed1979

Insulin-dependent diabetes and HLA.

The study of a hundred and fifteen unrelated insulin-dependent diabetes and eight families with at least two insulin-dependent diabetes members made it possible to confirm the higher frequency of HLA-B8 and B18 (p less than 0.001) among patients, producing a RR of 2.24 and 2.47 respectively. The increased B15 frequency did not achieve statistical significance. B18 whose gametic association (delta = 0.0438) was significant only in diabetic patients was often related to Aw19-2 (Aw30 + Aw31). The B8/B18 genotype gave a relative risk (RR = 4.98) which was significantly higher than that of B8, B18 and B15 heterozygotes (1.50, 1.24 and 1.39 respectively). Pairs of diabetic siblings were more frequently HLA identical than would be expected by chance, and distribution of the pairs of affected sibs into the three categories, identical, semi-identical and different, was closer to the recessive model than to the dominant one. The fact that the B8/B18 individuals had a RR slightly higher than the B8 and B18 homozygotes and distinctly higher than the heterozygotes for only one of these genes, favours the hypothesis of two dominant genes, giving the appearance of recessivity. The gene associated with B18 in Southern Europe seems to play the same part as that of the gene associated with B15 in Northern Europe.

Adolescent↗
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↗
PubMed1978

The role of HLA-DR antigens in transplantation--survival of skin allografts in HLA-haploidentical donor-recipient combinations.

The results of 79 skin grafts performed in haploidentical donor-recipient pairs are correlated with HLA-A, -B, -C, and -DR compatibility. A strong detrimental effect of DR incompatibilities has been demonstrated. This effect is independent from that exerted by products of the HLA-A, -B, and -C loci. An additive effect of HLA-A, -B, and -DR incompatibilities on allograft survival time has been observed.

Chromosome Mapping↗
PubMed1977

HLA B27 and ankylosing spondylitis: a population and family study in Sardinia.

Thirty-eight patients with ankylosing spondylitis (AS) and 494 unrelated controls in Sardinia were HLA Typed. HLA B27 was present in 81.8 per cent of AS vs 5.3 per cent of controls (relative risk: 80). Twenty-six apparently healthy B27 positive individuals were studied clinically and radiologically, and six (23.0 per cent) presented signs of definite or suspicious AS. A family study on relatives of seven AS B27-positive and four AS B27-negative patients was also made. The results suggest a dominant heredity of AS susceptibility, and are compatible with a direct involvement of the B27 antigen in the mechanism of AS, but we cannot rule out a closely linked disease-susceptibility gene with incomplete penetrance.

Adult↗
PubMed1977

[Excess of HLA-A2 and HLA-A2 homozygotes in patients with aplastic and Fanconi's anemias].

In 68 idiopathic aplastic anemia patients (65 HLA genotypes), HLA-A2 is slightly increased (p corrected less than 0.03) leading to a relative risk of 2.30. A slight excess of homozygotes for HLA-A was observed (22.2 vs. 14.09%), involving mostly the A2 antigen. In the siblings the patients were more frequently homozygote A2 than by chance (p less than 0.005). The same trends are observed in Fanconi's anemia = out of 18 patients, 7 are HLA-A homozygote (of whom 4 are A2). The hypothesis of the existence of one or several recessive genes involved in hematopoiesis situated close to HLA-A is advanced.

Anemia, Aplastic↗
PubMed1977

HLA antigens in Sardinian patients with diabetes mellitus.

HLA-B8 and HLA-Bw15, two antigens associated with juvenile diabetes mellitus in Caucasians of North Europe, have a very low frequency in Sardinian population, who nevertheless have a high frequency of diabetes. The association between diabetes and HLA in Sardinian population has therefore been investigated in 60 patients with diabetes, mellitus (32 with juvenile diabetes and 28 with maturity onset diabetes) and 96 normal, unrelated random controls. No disturbance of HLA distributions was found in maturity onset diabetes, but the frequencies of B8 and Bw35 were increased among juvenile diabetics (18.7 percent and 28.1 percent respectively, compared with 2.0 and 11.4 percent in healthy controls). B18 antigen frequency was also increased, although not significantly, in juvenile diabetes mellitus (65.6 percent compared with 50 percent in controls). In contrast the frequency of HLA-Bw15 in two groups of diabetics differed little from that of controls.

Adult↗
PubMed1975

Hl-A antigens associated with rheumatoid arthritis and ankylosing spondylitis in an ethnic homogeneous population.

The HL-A phenotypes of 52 patients with rhematoid arthritis and 26 patients with ankylosing spondylitis from an ethnic homogeneous population have been determined. No definite association has been established with rheumatoid arthritis, while a very significant association has been found between ankylosing spondylitis and HL-A 27 antigen. This finding suggests that certain patients with ankylosing spondylitis have a genetically determined susceptibility to their disease which could be due to a cross-tolerance mechanism enabling infectious agent antigens to mimic certain histo-compatibility antigens, or to a linkage between HL-A genes and those controlling immune responsiveness.

Arthritis, Rheumatoid↗