Interleukin 3 can compensate for the deficiency in erythroid burst-forming cells in anemic mice of genotype W/Wv.
Bone marrow cells from mice with the W/Wv mutation have about one-third the erythroid burst-forming cells (BFU-E) found with wild-type littermates. The mutant cells are also less responsive in vitro to exogenous erythropoietin (epo) than are the wild-type cells. Addition of interleukin 3 (IL-3) to the culture medium largely corrects the deficit in burst formation and in responsiveness to epo. When mutant cells are incubated for 2 days in the absence of epo but with IL-3 present, burst formation is the same as with wild-type cells, suggesting that IL-3 acts on maintenance in vitro and/or proliferation of primitive precursor cells of both mutant and wild-type mice.
Goldwasser
E
E
Department of Biochemistry and Molecular Biology, University of Chicago, IL 60637.
Pech
N
N
Ihle
J
J
D000818:Animals; D001854:Bone Marrow Cells; D002452:Cell Count; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D004351:Drug Resistance; D015672:Erythroid Precursor Cells / Q000166:cytology*; D004921:Erythropoietin / Q000494:pharmacology; D005260:Female; D007377:Interleukin-3 / Q000494:pharmacology*; D051379:Mice; D008817:Mice, Mutant Strains; D011994:Recombinant Proteins / Q000494:pharmacology
D007377:Interleukin-3; D011994:Recombinant Proteins; D004921:Erythropoietin