ISSN:
1744-313X
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Biology
,
Medicine
Notes:
CBA/N mice have an X-linked B cell defect which prevents them from responding to non-mitogenic thymic independent (TI-II) antigens such as dinitrophenylated (DNP-AGG) Ficoll. The F1 male progeny of CBA/N female mice express the same defect. Spleen cell suspensions from such defective mice (CBA/N X C3H/HeN F1 males) could not respond to DNP-AGG-Ficoll following in vitro immunization and subsequent transfer into irradiated, syngeneic, F1 male recipients as expected. In contrast, normal CBA/N X C3H/HeN F1 female spleen cells could respond and effect a ‘rescue'; they mounted strong plaque-foriming cell 7 days after in vitro exposure to DNP-AGG-Ficoll and subsequent transfer into irradiated F1 male recipients. Defective F1 male spleen cells could bind significant quantities of DNP-AGG-Ficoll, however, after, in vitro exposure. Extensive washing of these spleen cells could not reverse this binding. Such DNP-AGG-Ficoll-exposed and washed F1 male spleen cells could, after transfer, aid normal untreated F1 female cells in their rescue function. The defective F1 male spleen cells could convey immunogenic quantities of DNP-AGG-Ficoll to the ‘rescuing’ F1 female cells.Mitomycin treatment of F1 male cells did not interfere with their conveyor function. Goat anti-mouse μ serum impeded the passive antigen conveyor function of defective F1 male cells as did prior exposure to high concentrations of free DNP-AGG hapten. Our data support the view that the B cell defect of CBA/N X C3H/HeN F1 male mice does not relate to antigen binding, but rather to an inability to be effectively triggered by certain cell-bound polymeric antigens.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1744-313X.1980.tb00735.x
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