Expression of an X-linked gene family (XLR) in late-stage B cells and its alteration by the xid mutation View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1985-03

AUTHORS

David I. Cohen, Alfred D. Steinberg, William E. Paul, Mark M. Davis

ABSTRACT

One of the most extensively studied X-linked immunodeficiency disorder is the xid mutation of the mouse strain CBA/N (reviewed in ref. 1). This mutation may involve a maturational defect as xid animals are unable to raise antibodies to soluble polysaccharide antigens, a function normally attributed to late-stage B cells2,3. Moreover, studies using monoclonal antibodies have defined a B-cell surface antigen (BLA-2 or 14G8) that is expressed on most or all immature B lymphocytes, but not on a subpopulation of mature splenic B lymphocytes4,5; this late-stage, 14G8 antigen-negative splenic B-cell subpopulation is apparently absent from mice bearing the xid defect5. In the accompanying paper6 we describe the isolation of a cDNA clone recognizing a family of genes on the X chromosome, at least some of whose members are closely linked to the xid trait. We report here that this gene family, XLR, is transcribed in certain B- and T-cell lineage tumours, but not in macrophage tumours, or liver or kidney cells. We show that it is transcribed principally in late-stage, 14G8-negative B-cell tumours and plasmacytomas, but not in immature B-cell or pre-B-cell tumours. We are able to detect transcription in all of 12 plasmacytomas (secretory B-cell tumours) derived from mice with normal X chromosomes, but not in three plasmacytomas carrying the xid mutation. These data, combined with the restriction fragment length polymorphism analysis linking the XLR gene family to the xid mutation6, suggests that the xid defect occurs within a member of this gene family. More... »

PAGES

372-374

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/314372a0

DOI

http://dx.doi.org/10.1038/314372a0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1022461001

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/3872416


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