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Biomedical subjects

M Sasportes

Publications and source records attributed to M Sasportes.

At least 19 recordsLinked to original sources

[Demonstration of a soluble factor capable of inhibiting allogenic lymphocyte proliferation in man].

During the secondary mixed lymphocyte reaction (MLR), i.e. after the double in vitro allogenic sensitization between responding and stimulating cells bearing at least one HLA-DR incompatibility, suppressor cells are developed [1]. They are able to inhibit a primary MLR provided that the stimulating cells possess the same DR incompatibility as the immunizing cells. We report here that this inhibition is due to the production by these cells of a soluble suppressor factor which acts on responding cells provided that they share at least one gene product of the HLA-D region with the cells producing the factor. This a feedback process of auto-inhibition occurring after hyperimmunization. The action of this suppressor factor seems to be genetically restricted to an as yet unknown locus in linkage disequilibrium with HLA-DR.

Cell Division

Regional mapping of the HLA on the short arm of chromosome 6.

A detailed gene marker study was performed on a partial 6p trisomic child resulting from a balanced maternal translocation t (2;6) (p 2505; p2105). HLA typing and mixed lymphocyte reaction showed that the breakpoint on chromosome 6 was located within the HLA gene cluster, allowing an accurate location of the D determinants. Localization of the P blood group locus within the region 6 p 2105 to 6 p ter was excluded.

Cells, Cultured

Hereditary C2 deficiency associated with common variable immunodeficiency.

Homozygous C2 deficiency in a 19-year-old boy was associated with variable immunodeficiency manifested by marked hypoimmunoglobulinemia and impaired antibody responses, normal circulating B lymphocytes, and subnormal T-cell functions. Neither antilymphocytic autoantibodies nor chromosomal abnormalities were found. Serum immunoglobulin levels were within normal limits in his parents and brother who were heterozygous for C2 deficiency. The patient's lymphocytes were homozygous at the HLA-D locus but expressed an antigen different from DW2.

Adult

Human Ia-like DRw lymphocyte antigens stimulating activity in primary mixed lymphocyte reaction.

The intensity of the primary mixed lymphocyte reaction (MLR) seems to be influenced by at least two distinct determinants of the HLA-D region: the HLA-Dw stimulating products and the human Ia-like B lymphocyte DR (D-related) antigens. In three families, the primary MLR is significantly higher in case of HLA haploidentity, when stimulating and responding cells differ with regard to both Dw and DRw determinants, than when only Dw products are different. Thus, an additional effect of DR antigens during primary MLR is observed. The role of DRw antigens in primary MLR and the results obtained by a primed lymphocyte test which can discriminate between Dw3 and DRw3, indicate that DRw and Dw products could be distinct determinants.

Epitopes

HLA-DR-specific suppressor cells after repeated allogeneic sensitizations of human lymphocytes in vitro.

In conclusion, DR-specific suppressor cells can be induced by repeated in vitro sensitizations. They were able (1) to decrease a secondary proliferation, (2) to suppress consistently, in a primary proliferative assay, when added as third cells (primed twice against a DR antigen [PLT II] and gamma-irradiated), the response of unprimed cells towards stimulating cells, which share a DR specificity with the priming cell of the PLT II. The suppression follows the D part of the recombinant haplotype within an HLA-B/D recombinant family and is specific for the DR antigen used twice as stimulator for production of the PLT II.

Epitopes

[Hereditary C2 deficiency with systemic lupus erythematosus: clinical and immunologic studies in a family (author's transl)].

A case of systemic lupus erythematosus associated with an homozygous deficiency in the second fraction of complement is reported and compared to previous reports of the literature. The high incidence of infections in these patients is outlined. The defective gene in this family was associated with the HLA A10B18 haplotype and the propositus was homozygous at the HLA-D locus. Familial study allowed the detection of 3 heterozygous individuals two of them being symptomatic (vascular purpura, high incidence of bacterial infections).

Adolescent

[Close genetic relation between determinants coding for the HLA-D region, detected by the technique of mixed primary and secondary lymphocyte culture and by serology of B lymphocytes].

In this study we report that: 1. Li determinants serologically detectable or closely linked structures are more associated to secondary responses than HLA-D specificities defined by HTC testing; 2. Other determinants from loci, MHC linked, or cross reactivity between Li determinants must be postulated to explain discrepancies between secondary responses and B serology; 3. Li determinants have an effect on the intensity of the reaction in primary allogenic proliferation.

Adult

[Detection of a minor stimulating product involved in secondary allogenic proliferation of human lymphocytes in vitro].

In a family with a shared parental haplotype studied in MLR I and II we report that: 1) A secondary proliferation can be induced without a primary positive MLR; 2) In these conditions a minor determinant activating secondary proliferation is detected; 3) No significant association of this product with the available makers (HLA-A, B, C, D, Ly-Li) of the HLA region has been found so far; its localisation within or outside the MHC is under investigation.

Adult

Suppression of generation of human cytotoxic effectors by lectins or lectin-activated peripheral blood lymphocytes.

The lectins phytohemagglutinin, pokeweed mitogen and concanavalin A used at their optimal mitogenic concentration, or human lymphocytes activated by the same mitogens, were found to suppress the in vitro generation of cytotoxic effectors when added to a cell-mediated lympholysis (CML) mixture during the first 48 h of culture. The data suggest that the suppressive mechanism is mediated to a greater extent by an allogeneic interaction between lectin-activated cells and the allogeneic cells present in the CML mixture than by suppressor cells induced by the lectin. Since partial suppression was observed with supernatants of activated lymphocytes cultured for 18 h with allogeneic stimulating cells (but not activated lymphocytes alone), a soluble mediator may be involved in the suppressive mechanism. The mechanism of suppression therefore may be identical to the preemption phenomenon recently described in primary and secondary CML.

Antigens

Detection of HLA-D clusters using primed LD typing.

Using a set of 17 primed LD typing (PLT) cells tested on a panel of 35 unrelated cells, we showed that certain groups of PLT cells tended to detect similar unrelated cells. The PLT cells were grouped into seven clusters and these tended to correlate with the seven HLA-D specificities represented on the panel, as determined by HTC testing. These data suggest that the antigens that cause restimulation in PLT are similar to those HLA-D antigens detected by the homozygous typing cell (HTC) test or, alternatively but more unlikely, that the two typing methods are detecting genes in close linkage disequilibrium with the HLA-D region.

Epitopes

Detection by three cellular immunological techniques of the antigenic determinants of the Ly-Li system, expressed on human B lymphocytes.

A clear correlation was observed between the presence of an Ia-like antigenic B-cell system Ly-Li, detected serologically, and three cellular immunological techniques: [1] mixed lymphocyte reaction (MLR) inhibition by an anti-Li antiserum; [2] level of restimulation of anti-Ly-Li in-vitro-primed lymphocytes; and [3] detection of HLA-D alleles by homozygous typing cells. These results suggested that the allelic products detected serologically may be identical to those detected by the first two techniques, namely MLR inhibition and in-vitro-primed lymphocyte typing, and, possibly, HLA-D typing using homozygous typing cells, although the correlation was repeatedly found to be less clear for the last technique.

B-Lymphocytes

Detection of HLA-D clusters and segregation studies using primed LD typing.

By testing a group of PLT cells over a panel of unrelated restimulating cells, the PLT's could be grouped into clusters according to their ability to discriminate antigen(s) in unrelated cells. The PLT clusters broadly correlated with the homozygous typing cell-defined HLA-D clusters represented on the panel. The PLTs grouped together clearly segregate with a particular HLA haplotype when tested in both unrelated families not possessing the sensitizing haplotype and in the family with the sensitizing haplotype. No influence of HLA SD antigens could be observed in PLT restimulation in the segregation studies.

Epitopes