Deficient transformation of murine trisomy 16 fetal liver cells by the Abelson and J2 viruses.

Abstract:

:Mouse trisomy 16 (Ts16), an animal model for human Down syndrome (trisomy 21), exhibits severe abnormalities in the development of lymphoid and myeloid cells. Whereas fetal liver cells from diploid mice can be easily immortalized by retroviral transformation with Ab1-MuLV or J2 virus, fetal livers from Ts16 mice contain significantly fewer transformable cells. Infection of Ts16 fetal liver cells by Ab1-MuLV results in a 52- and 12-fold reduction in the frequency of transformation at days 17 and 18 of gestation, respectively. By contrast, the efficiency of transformation with J2 virus, another retrovirus known to transform fetal liver cells, is only mildly (factor 2-3) affected. The Ig gene rearrangements of Ts16 and diploid retrovirally transformed fetal liver cell lines do not differ from one another. This suggests that there is a deficiency in the early stem cell compartment, rather than in the development of pre-B cells.

journal_name

Immunol Lett

journal_title

Immunology letters

authors

Berger CN,Epstein CJ

doi

10.1016/0165-2478(92)90092-3

subject

Has Abstract

pub_date

1992-06-01 00:00:00

pages

47-51

issue

1

eissn

0165-2478

issn

1879-0542

pii

0165-2478(92)90092-3

journal_volume

33

pub_type

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