Previous studies in this laboratory revealed that NZB mice have abnormalities of myeloid progenitor populations from an early age such that they are poorly responsive to a particular type of colony-stimulating activity (CSA). In addition, these mice develop abnormally high numbers of B cells that can be cloned in semisolid agar cultures and that are atypical in resisting inhibition by anti-mu antibodies. To investigate whether these abnormalities, like other autoimmune phenomena studied previously, are transferrable with hemopoietic cell grafts, we performed reciprocal bone marrow transplants between NZB and normal DBA/2 mice. Irradiated control mice given syngeneic marrow did not change with respect to any of the parameters that were measured. In contrast, DBA/2 recipients of NZB marrow were indistinguishable from NZB mice in terms of CSA responses and incidences of anti-mu resistant B cells. The proportions but not total numbers of clonable B cells ere elevated in these mice until at least 16 wk after grafting. Conversely, NZB mice given DBA/2 cells had all of the normal characteristics of DBA/2 mice. Transplantation did not cause significant changes in hematocrits, reticulocyte counts, or spleen weights. Therefore, all elements necessary for expression of these lymphoid and nonlymphoid abnormalities of NZB mice are intrinsic to radiosensitive hemopoietic cells.