A fusion protein containing a B cell lymphoma idiotype (Id) variable genes from the tumor and the preparation of and granulocyte-macrophage colony-stimulating factor tumor-specific vector constructs. The low production of (GM-CSF) is a potent stimulator of tumor immunity. In three Id/GM-CSF fusion proteins by transfected cells, which is different tumor models we show that immunization with a major obstacle in the use of purified fusion proteins for autologous lymphoma cells that have been engineered to immunotherapy, is due to the presence of the cytokine express the Id in the context of GM-CSF is much more gene in the immunoglobulin locus. Low production, howeffective than immunization with an equivalent dose of the ever, is not limiting in the cell-based setting, because upon purified protein. The lymphoma Id could be modified by in vivo administration of the modified autologous cells, introducing the GM-CSF gene into the immunoglobulin (Ig) even minute expression levels are sufficient to induce heavy chain locus via gene targeting. This approach cirtumor immunity. cumvents the isolation of the rearranged immunoglobulin
A codominantly inherited mutation of the lactate dehydrogenase (LDH) in the C3H mouse causes a severe hemolytic anemia in homozygous mutants, whereas viability and fertility are close to normal. Investigation of multipotent hemopoietic stem cells (CFU-S), myeloid (GM-CFC) and erythroid progenitors (BFU-E, CFU-E) in femur and spleen indicates a general shift from bone marrow to splenic hemopoiesis. In terms of total body hemopoiesis, however, the BFU-E pool is 1.4- and the CFU-E pool 19-fold enlarged, whereas CFU-S and GM-CFC show little or no deviation from normal. It is concluded that this mouse mutant is an appropriate model of long-term hemopoietic stress showing that compensation in this severe hemolytic anemia is achieved primarily by an increase of the number of the most mature erythroid progenitors.
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