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D Pious

Publications and source records attributed to D Pious.

46 records · Page 3Linked to original sources
PubMed1977

HLA variants of cultured human lymphoid cells: evidence for mutational origin and estimation of mutation rate.

Variants of a diploid lymphoid cell line that show a loss of HLA-B27 antigen occur randomly in time and independently of exposure to the alloantiserum used for their isolation. From these and previous findings of variant stability, inducibility by mutagens, and the absence of linked variation, we colclude that most HLA variants arise by mutation. The mutation rate for HLA-B27 loss is 8 x 10(-7) per cell per generation.

B-Lymphocytes↗
PubMed1976

Isolation of stable and unstable ("suppressed") Beta2-microglobulin-deficient clones from a lymphoid cell line.

After selection with anti-Beta2m and C against a human lymphoid line, about 10% of surviving clones manifested decreased cytotoxic sensitivity to anti-Beta2m("suppression") which gradually reverted to normal after 35 to 55 cell doublings. Antiserum alone induced suppression. Exposure of suppressed clones to DMSO substantially reversed suppression. One clone, surviving selection, had a stable decrease in anti-Beta2m sensitivity; it possibly represents a Beta2m mutation.

Beta-Globulins↗
PubMed1973

Isolation and characterization of HL-A variants in cultured human lymphoid cells.

We have developed a procedure for immune selection in an established human lymphoid cell line based on HL-A, the major human histocompatibility locus. After a single brief exposure to selective conditions, HL-A2 variant clones were isolated from an HL-A2/HL-A3 heterozygous line. The variant clones occurred at a frequency of about 1 x 10(-6). The variant phenotype was stable during prolonged growth in the absence of antiserum after isolation. The variant sublines bound [unk] 1/1000 the HL-A2 antibody per cell as the parent line. Variation was specific in that expression of antigens not selected against was unimpaired. Loss of the chromosome bearing HL-A2 was excluded as the cause of variation because the variants, like the parent line, were heterozygous for phosphoglucomutase (EC 2.7.5.1) determined by structural locus PGM(3), which is linked to HL-A.

Animals↗
PubMedDate not supplied

A gene in the human major histocompatibility complex class II region controlling the class I antigen presentation pathway.

Major histocompatibility complex (MHC) class I molecules export peptides to the cell surface for surveillance by cytotoxic T lymphocytes. Intracellular peptide binding is critical for the proper assembly and transport of class I molecules. This mechanism is impaired as a result of a non-functional peptide supply factor gene (PSF) in several human mutant cell lines with genomic lesions in the MHC. We have now identified PSF in the MHC class II region by deletion mapping in mutants and chromosome-walking. PSF is homologous to mammalian and bacterial ATP-dependent transport proteins, suggesting that it operates in the intracellular transport of peptides.

Amino Acid Sequence↗