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12 July 2008 The role of adherent cells in the immunosuppressed state of mouse progeny transplacentally exposed to benzo(α)pyrene
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In recent studies, we showed that murine fetal liver cells from progeny exposed to benzo(α)pyrene in utero by intraperitoneal injection of the dam at midpregnancy (12 d) suppressed cell proliferation in an allogeneic mixed lymphocyte response. On the other hand, fetal liver cells from the corn oil (vehicle for the carcinogen)-exposed progeny (control) appeared to enhance proliferation. Suppression or enhancement appeared to be mediated by fetal liver bearing CD8 and Lyt 1 (CD5 ) cells. Despite these manifestations, the role of third-party cells needs to be considered. As a first premise, adherent cells were targeted as possible third-party cells. To test the role of the adherent cells, liver cells from benzo(α)pyrene-exposed fetuses were treated with ficoll-hypaque, and the interface cells were fractionated through glass wool or nylon wool. It is known that adhering cells, macrophages and B cells, readily attach to glass or nylon wool. The effluent cells and the adherent cells were cultured with syngeneic responder cells and allogeneic stimulator cells in a mixed lymphocyte response. The results showed that benzo(α)pyrene-effluent cells led to the enhancement of proliferation in the mixed lymphocyte response, while benzo(α)pyrene-adherent cells led to suppression. The effluent and adherent cells of corn oil controls did not modify cell proliferation in the mixed lymphocyte response. These data suggest that a third-party cell, reasonably the macrophage or possibly B cells or both, since these are adherent cells, play a decided role in mediating suppression in the benzo(α)pyrene-exposed progeny.

Paul Urso and Mary K. Kramer "The role of adherent cells in the immunosuppressed state of mouse progeny transplacentally exposed to benzo(α)pyrene," In Vitro Cellular & Developmental Biology - Animal 44(7), 273-279, (12 July 2008).
Received: 5 November 2007; Accepted: 10 April 2008; Published: 12 July 2008

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