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Biomedical subjects

M S Pollack

Publications and source records attributed to M S Pollack.

At least 127 records · Page 7Linked to original sources
PubMed1980

Histocompatibility testing for clinical bone marrow transplantation and prospects for identification of donors other than HLA genotypically identical siblings.

Clinical histocompatibility testing has now developed to a stage where it is possible to select related bone marrow donors for some patients, when HLA genotypically identical siblings are not available. The most common type of such donors are the HLA phenotypically or HLA-D phenotypically identical related donors. The HLA-D homozygous recipient offers special options, since these patients can potentially receive bone marrow transplants from any of the parents or from HLA-haploidentical siblings. The studies in SCID have demonstrated that HLA-D compatibility in spite of HLA-A or B incompatibilities can be tolerated and there is now accumulating evidence that even patients with aplastic anemia or acute leukemia can be successfully treated with such bone marrow grafts.

Bone Marrow Transplantation↗
PubMed1980

Different HLA antigen associations for the functionally active and inactive products of the complement C4F1 allele.

The genetic polymorphism of the fourth component of human complement, C4, was studied in 945 unrelated Caucasian individuals. A third allele of the C4F (Rodgers) locus, termed C4F1 was demonstrated. This allele is characterized using immunofixation electrophoresis, by the presence of an additional fast-moving anodal band of C4 which distinguishes it clearly from the common C4F variant. The allelic frequencies fit the Hardy-Weinberg equilibrium assuming three alleles at the C4F locus: C4F, C4Fo, and C4F1. The functional activity of the C4F variants was investigated using a specific hemolytic overlay technique for C4. It was found that in almost all individuals (75 out of 78), the C4F1 allele codes for a functionally inactive C4 product only when it occurs on an HLA-B17 positive haplotype but that the same allele codes for a functionally active fast variant of C4 when it occurs on an HLS-B37 positive haplotype (18 out of 18). Very strong genetic linkage disequilibrium was observed for the C4F1 allele with HLA-B17 and B37. The active and inactive C4F1 variant also has marked nonrandom gametic association to different alleles of the Bf locus and to HLA-C locus determinants. No further variants of the C4S (Chido) locus have been identified so far. Rodgers (Rg) typing by the plasma inhibition test of anti-Rg antiserum has shown that plasma from individuals homozygous for the C4F1 allele is only able to partially inhibit anti-Rg whereas all C4F positive individuals totally inhibited the reaction.

Alleles↗
PubMed1980

HLA-linked B cell alloantigens of a new segregant series: population and family studies of the SB antigens.

In order to define the new human histocompatibility antigens, we have generalized primed lymphocytes using responder and stimulator cells matched for all recognized HLA-linked histocompatibility antigens (A,B,C,D,DR,MB). Many such primed lymphocytes give highly discriminatory proliferative responses specific for antigens which differ between HLA-A,B,C,D,DR, and MB matched restimulating cells. Five distinct antigens have been defined which appear to be part of a single segregant series (designated "SB"). Studies in a DR/GLO recombinant family indicate that the antigens are coded by an HLA-linked gene telomeric to GLO. Family studies of 57 HLA haplotypes provide an estimate of genotype frequency which is 12% or less for four of the SB alleles but approximately 50% for the most common (SB4, which may be a "public: determinant); approximately 25% of haplotypes are blank. Population studies of one of the SB antigens (SB1) suggest that it is in linkage disequilibrium with the SB antigens are part of a highly polymorphic new segregant series of B cell alloantigens encoded by a gene that maps between HLA-B and GLO.

B-Lymphocytes↗
PubMed1980

Frequency of alloantibodies reacting with PHA-activated T lymphocytes, unexplainable by known HLA activities.

Two hundred and three sera obtained from multiparous women were screened to determine the frequency of the appearance of antibodies reactive with PHA-activated T lymphocytes, but not with resting B or T cells from the same donor. The panel of cells on which the sera were tested consisted of lymphocytes from 38 unrelated donors known to be homozygous at the HLA-D locus. Forty-two sera were shown to react uniquely with PHA-activated T cells. The reactivities of these sera could not be explained in terms of the defined HLA-A,-B,-C, or DR antigen specificities on the panel cells, nor on the basis of known cross-reactivities among these antigens. Most of the antisera showed strong cytotoxicity with the activated T cells. Such sera may define antigens presented to the maternal immune system during differentiation and development, which are not expressed on adult T cells unless they are activated.

Animals↗
PubMed1980

DR-positive maternal engrafted T cells in a severe combined immunodeficiency patient without graft-versus-host disease.

A 2 1/2-year-old male infant with severe combined immunodeficiency was documented by HLA typing and the presence of a female karyotype in the few spontaneously dividing cells to have an intrauterine-derived maternal lymphocyte graft. The presence of DR antigens on the engrafted maternal E rosette-forming T cells was demonstrated by both cytotoxicity and immunofluorescence techniques using both conventional and monoclonal antihuman DR antisera. These DR antigens were of the same allospecificity, DR4, as the mother's peripheral blood B cells. The patient's B cells and monocytes expressed DR alloantigens DR4 and DR3, corresponding to his genotype. Although fresh maternal lymphocytes react strongly in vitro against patient non-T cells, the engrafted maternal T lymphocytes no longer show this activity. Furthermore, clinical evidence suggesting mild graft-versus-host disease was completely resolved by the end of his first year. The presence of the DR-positive maternal cells may reflect the survival of a group of activated suppressor cells mediating graft tolerance of host tissue.

Child, Preschool↗
PubMed1980

Distribution of HLA antigens in patients with Ewing's sarcoma.

Thirty-eight unrelated Caucasian patients with Ewing's sarcoma were typed for HLA-A and B locus antigens. Although no significant differences in the distribution of these antigens were found in comparison with local controls, a trend towards increases in LHA-B8 and Aw19 complex antigens was noted. Although American blacks are only rarely affected by this tumor, the two black patients we typed both had the HLA-Aw19 complex antigen, Aw31. This suggests that a disease susceptibility factor may be in linkage disequilibrium with HLA-Aw19 complex HLA antigens.

Adolescent↗
PubMed1980

Genetically appropriate expression of HLA and DR (IA) alloantigens on human melanoma cell lines.

Studies of the expression of HLA and DR alloantigens on cultured human melanoma cells in comparison with those expressed on peripheral lymphocytes and B-cells derived from the same patients have shown that the HLA-A,B, and C locus antigens expressed on the cultured tumor cells were consistent with those expected from the typing of peripheral blood lymphocytes. One melanoma cell line failed to express all the HLA antigens expected from donor typing. All five of the lines tested also expressed DR antigens and in three instances these could be demonstrated to have genetically consistent allotypes. However, in preliminary studies stimulation of allogeneic lymphocytes by the DR positive melanoma cells could not be demonstrated.

Aspartate Aminotransferases↗
PubMed1980

Fatal graft-versus-host disease following blood transfusion in Hodgkin's disease documented by HLA typing.

Fatal graft-versus-host disease (GVHD) developed in a patient with Hodgkin's disease treated with combined chemotherapy and radiotherapy following the transfusion of 2 U of packed red blood cells. Clinical features of the GVHD included the development of exfoliative dermatitis, progressive hepatic dysfunction, aplastic anemia, and finally progressive fatal pneumonia. GVHD was documented by skin biopsy and chimerism by HLA typing. The HLA phenotype of the patient's skin fibroblasts [A3, Bw44 (w4)/A2, B15 (w4)] was appropriate for parental haplotypes and probably represented her true HLA phenotype. Lymphocytes from the patient (peripheral blood and lymph node biopsy) were of a different HLA phenotype (A3; Bw35, w38, w4, w6; Cw4), which was inappropriate for parental HLA haplotypes but identical to the HLA phenotype of one of the blood donors. The HLA-DR typing of the patient's family and of the blood donor demonstrated that the patient and the donor probably were HLA-DR identical (DRw5/DRw6), although no B lymphocytes could be obtained from the patient for direct DR typing. We are currently irradiating all blood products administered to patients with Hodgkin's disease receiving intensive treatment. Further observations will be necessary to determine whether transfusions to other cancer patients with immunodeficiency states should be restricted to irradiated blood products.

Adolescent↗
PubMed1979

Prenatal diagnosis of congenital adrenal hyperplasia (21-hydroxylase deficiency) by HLA typing.

Congenital adrenal hyperplasia (C.A.H.) due to 21-hydroxylase deficiency is an HLA-linked recessive disorder. HLA-A and B antigens are expressed on amniotic cells. Prenatal diagnosis of C.A.H. by HLA typing of families and amniotic cells was attempted in two at-risk families. In one family HLA typing indicated that the fetus would have C.A.H., and this prediction was confirmed after birth. In the second family, HLA typing indicated that the fetus would be an unaffected, phenotypically normal carrier of the disease gene, and this prediction was also confirmed after birth.

Adrenocortical Hyperfunction↗
PubMed1979

HLA-DR antigens in Black North-Americans and their association with HLA-D.

A random population of 108 Black North-Americans, 79 of whom had also been typed for HLA-D in Mixed Leukocyte Culture (MLC), were serologically tested for DRw with Seventh International Histocompatibility Workshop trays. Clusters of B cell alloantisera were identified which defined several DRw antigens. Although the clusters for DRw1, DRw2, DRw3 and DRw7 showed similarities with the clusters derived during the Seventh International Histocompatibility Workshop, distinct differences were observed which should be taken into account for the assignment of the DRw antigens in Blacks. DRw6 was defined by a cluster of sera which also reacted with DRw1 and DRw2 cells. The tails of these sera were used to assign DRw6, but this was only possible with DRw1 and DRw2 negative cells. It was not possible to identify serum clusters specific for DRw4 or WIA8. The associations between DRw and the corresponding Dw specificities were reasonably good for DRw1, DRw2 and DRw7, but weaker for DRw3 and DRw5. The cumulative gene frequencies for DRw1, DRw2, DRw3, DRw5, DRw6 and DRw7 was 0.86. The frequencies of these six DRw antigens fitted into a Hardy-Weinberg distribution, suggesting that DRw in Blacks is controlled by a single gene with multiple alleles.

Black People↗