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C57BL/6J mice were treated with ALS, ALG, normal rabbit serum (NRS) or IgG of the rabbit for a period of 6 days To study the xenogeneic antigenicity of ALG and its antilymphocytic effect separately, half the mice were made tolerant to IgG of the rabbit. While a short schedule of injections of ultracentrifuged lgG induced tolerance to IgG, this tolerance was eliminated by the subsequent treatment with ALG. A prolonged injection schedule over 44 days did, however, lead to a tolerance which persisted after ALG treatment. [131]IgG elimination proved to be a more sensitive control of tolerance than immunodiffusion. Semiquantitative cytology revealed a decline in lymphocytes, erythroblasts and megakaryocytes in the bone narrow and erythroblastosis and megakaryocytosis in the spleen. Cells of the myeloid series invariably increased in number. The effect on erythroblasts persisted after removal of contaminating haemagglutinins. ALG-treated animals intolerant to IgG had about four times more splenic plasma cells than ALS-treated mice tolerant to IgG. The 6 days' treatment with ALS reduced the, absolute number of nucleated bone marrow cells by 16% and doubled the spleen indices. Under this treatment, relative and absolute cell counts revealed an ALG-induced shift of erythroblasts, megakaryocytes and perhaps also of plasma cells from the bone marrow to the spleen. The effect of NRS or IgG was similar to that of ALS or ALG but remained on a lower level. The remarkable changes in the histologic structure of the splenic follicles after treatment were almost completely reversed by a prior induction of tolerance to IgG. [ABSTRACT FROM AUTHOR]

Cytology and histology of recipients of allogeneic bone marrow were studied 13, 20, 24, 30 and 34 days after transplantation. The developing chronic secondary disease was characterized by increased numbers of myeloid cells, by lymphopenia and by erythroblastopenia in the bone marrow and the spleen. Erythroblastopenia together with lymphopenia and augmented myeloid cells also occurred in irradiated F1-hybrids suffering from a chronic homologous disease. The latter model eliminated the following as a cause of erythroblastopenia in secondary disease: (I) host-versus-graft reaction against donor-type erythroblasts for immunogenetical reasons, and (2) graft-versus-host reaction against recipient-type erythroblasts since they had already been destroyed by irradiation. Treatment of the donor with ALS iesulicd iii a suppression of homologous disease in F1-hybrids with a cytology resembling that of recipients of syngeneic spleen cells. The same treatment only delayed the onset of chronic secondary disease in recipients of allogeneic bone marrow. These allogeneic recipients, in contrast to the F1-hybrid recipients, died with the typical morphology of a chronic secondary disease. In recipients of syngeneic bone marrow from donors treated with ALS, repopulation with lymphocytes was somewhat delayed and transient erythroblastosis in the spleen occurred 20 days after transplantation. [ABSTRACT FROM AUTHOR]

We have studied in BALB/c mice the hematological alterations of the host induced by the growth of tumor cells in diffusion chambers (DC) In this model, host-tumor interactions are only mediated by soluble factors. Tumor cells proliferate and grow in DC up to 15 days after implant. Our results show a reversal of the granulocyte-lymphocyte ratio in peripheral blood, with lymphopenia and a relative increase of myeloid progenitors in the bone marrow of mice bearing DC with M3 tumor cells (M3TC).