Stable integration of mouse DNA into Ia-negative human B-lymphoma cells causes reexpression of the human Ia-positive phenotype.
Author(s) -
John Guardiola,
Léonardo Scarpellino,
Giovanna Carrà,
Roberto S. Accolla
Publication year - 1986
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.83.19.7415
Subject(s) - biology , gene , raji cell , microbiology and biotechnology , phenotype , major histocompatibility complex , genetics , dna , human leukocyte antigen , human genome , fusion gene , genome , antigen , cell culture
RJ 2.2.5, a variant of the human B-lymphoma cell line Raji, does not express the HLA-DR, -DQ, and -DP class II (or Ia) histocompatibility antigens, as a result of a defect in the transcription of the corresponding genes. This defect is corrected after fusion of RJ 2.2.5 cells with mouse Ia-positive cells. Previous work showed that the trans-acting transcriptional activator supplied by the mouse cells is encoded by a locus on mouse chromosome 16. We show here that reexpression of human major histocompatibility complex class II genes by RJ 2.2.5 cells can also be achieved by stable integration of mouse genomic sequences into the RJ 2.2.5 genome after DNA-mediated gene transfer.
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