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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

BALB/c mice infected with Rowson-Parr virus, a lymphatic leukemia virus isolated from the Friend complex, undergo a rapid depression of antibody response. Spleen cells from these mice in culture show a similar deficit in the response to stimulation with sheep red cells and inhibit the reactivity of normal splenocytes. In an attempt to reverse this immunosuppression, near normal responses were obtained in vitro from infected splenocytes by increasing antigen dose, by adding E. coli lipopolysaccharide, or, more effectively, by cocultivating with small numbers of unfractionated or T cell-depleted peritoneal exudate cells (PC), whereas other manipulations proved ineffective. PC did not prevent the inhibition of normal splenocytes by infected spleen cells, but exhibited substantial restorative activity in vivo. In similar experiments, the immunosuppression exerted by the entire Friend complex could be reversed by PC in vitro but not in vivo. These results indicate that a functional deficit of macrophages may be partially responsible for the immunological impairment induced by leukemia viruses and suggest rational approaches to evaluate the relevance of this impairment to oncogenesis.
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PMID:Reversal of immunosuppression induced by murine leukemia viruses. 107 70

Friend virus induces a leukemia characterized by the proliferation of neoplastic hematopoietic cells believed to be erythroid precursors. In vitro studies were conducted with spleen cells from mice with terminal Firend leukemia in order to determine their capacity for leukocytic differentiation. Spleen cells were obtained from leukemic DBA/2 mice 1 to 2 days before anticipated death and cultured in the presence or absence of colony-stimulating activity (CSA). Growth in liquid culture in dissusion chambers was dependent on CSA and resulted in the generation of normally differentiated granulocytes and macrophages. Colony formation in agar was also dependent on CSA, and the cloning efficiency of leukemic spleen cells was found to be approximately 10 times normal. The colonies formed were composed of leukocytes, which appeared morphologically normal. Total in vitro colony-forming units per leukemic spleen exceeded normal by more than 300-fold, but cells elaborating CSA were decreased. Although it is uncertain whether the stem cells stimulated by CSA are "normal" or leukemic," it is clear that Friend leukemia has profound effects on the proliferation and differentiation of nonerythroid stem cells.
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PMID:Granulocytic stem cells in Friend leukemia. 108 68

Spleen antibody-forming cells of mice yield a 3- to 10-fold increase in their response to sheep erythrocyte antigen if they are acutely infected by lactate dehydrogenase-elevating virus. This early stimulation is replaced by a long-term inhibition of the antibody-forming cells as the viremia goes into its persisting chronic stage. These contrasting immunological phenomena are examined as contributing factors responsible for the enhancement by this virus of asparaginase (EC 3.5.1.1; L-asparagine amidolydrolase) therapy against leukemia in mice, and for the alteration of the susceptibility of mice to various neoplastic processes.
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PMID:Antibody-producing cells: virus-induced alteration of response to antigen. 108 81

Normal mice contain cytolytic cells with specificity for in vitro grown mouse Moloney leukemia cells. Such killer cells are most frequent in the spleens; lymph node and bone marrow contain less and thymus virtually no killer activity. Peak activity is found around one to three months of age. Spleen cells from genetically athymic mice are as active killer cells as those from normal mice of the same strain. Treatment with anti-theta serum plus complement followed by removal of adherent and surface Ig positive cells by filtration through anti-Ig columns will leave between 1-5% of the original spleen cell population from a normal mouse. These cells have the morphology of small lymphocytes and perhaps contain all of the total original killer activity of the spleen against the Moloney leukemia cells. Such killer enriched cells are devoid of T and B lymphocytes and largely fail to function in antibody induced, cell-mediated lysis against antibody-coated chicken erythrocytes. It is concluded that the spontaneous selective cytotoxic activity of normal mouse spleen cells against Moloney leukemia cells is exerted by small lymphocytes of yet undefined nature.
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PMID:"Natural" killer cells in the mouse. II. Cytotoxic cells with specificity for mouse Moloney leukemia cells. Characteristics of the killer cell. 108 18

To understand further the hematopoietic dyscrasias induced by a variant (a) of Rauscher leukemia virus (RLV), we used Escherichia coli endotoxin to stress the hematopoietic system of control and RLV/a-infected BALB/c mice. During the preleukemic stages of virus infection, there was slight splenomegaly without peripheral blood erythroblastosis. Granulocyte release and tissue mobilization mechanisms appeared unaffected by the RLV/a infection. Both RLV/a-infected and control mice reacted to endotoxin with peripheral granulocytosis and peritoneal granulocyte mobilization, though the circulating granulocyte levels in RLV/a-treated mice initially were lower than those in controls. Spleen of RLV/a-infected animals were larger than those of controls, but both responded to endotoxin with elevated numbers of granulocytes and erythroblasts. Since numbers of bone marrow erythroblasts in both groups of mice were decreased after endotoxin, stem cell competition and/or shunting of stem cells from marrow to spleen may have been involved. Endotoxin also induced rapid falls in hematocrit levels in both groups. These studies suggested that RLV/a-infected mice can be a model to study 1) erythropoietic dysfunction uncomplicated by defective granulopoietic release and tissue mobilization control mechanisms, and 2) progression of evolving granulocytic leukemia.
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PMID:Granulopoiesis in "preleukemic" mice with anemia induced by Rauscher leukemia virus, variant a. 110 69

Spleen cells from untreated young male and female C57BL/6 and C58 mice and of male C3H/He mice showed cytotoxic activity in vitro against BALB/c X-radiation-induced leukemia RL male 1 cells by 51Cr-releasing lymphocyte-mediated cytoxicity (LMC) tests, but old mice of these strains lacked LMC activity. In contrast, spleen cells from male and female AKR, BALB/c, and DBA/2 mice, and from female C3H/He mice had no appreciable LMC activity. The proportion of active cells in spleens from young (C57BL/6 times BALB/c)F1 or reciprocal hybrid mice was higher in females than in males. The specificity of the LMC reaction of RL male 1 cells, determined by LMC inhibition assays, was somewhat different from that of previously reported serologic X.1 tests. Thus the antigen detected by LMC has been tentatively designated X.1'. The main effector cells in this system were uncharacterized cells not adherent to glass surfaces or nylon-wool columns. These findings in RL male 1 leukemia extend the evidence for the presence of naturally occurring LMC. With the single unexplained exception of strain C3H/He, the LMC activity against RL male 1 cells, exhibited by untreated mice of various strains, corresponded with a previous classification of mouse strains immunologically as X.1 responders or as X.1 nonresponders according to their ability to reject X.1-positive leukemia cells.
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PMID:Natural occurrence of lymphocytes showing cytotoxic activity to BALB/c radiation-induced leukemia RL male 1 cells. 115 37

Infection of adult CBA mice with Rauscher or Moloney leukaemia virus concomitantly with caseination significantly accelerated spleen amyloid development in irradiated, bone-marrow protected mice, but had no effect on untreated, adult thymectomized or thymectomized irradiated mice. Spleen tissue of mice infected with Moloney virus had the highest titre in the mice with accelerated amyloid development.
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PMID:The effect of Rauscher and Moloney leukaemia virus on amyloid development in casein-treated CBA mice. 116 70

W/Fu rats were injected subcutaneously with low numbers of cells from the Gross leukemia virus-induced lymphoma, (C58NT)D, which induced transient tumor growth and regression (regressors), or with high numbers of tumor cells resulting in progressive tumor growth (progressors). Spleen cells from regressors had a significant reactivity in the mixed leukocyte tumor cell interation (MLTI), while spleen cells from progressors were unresponsive. Similarly, the responses to the non-specific mitogens, phytohemagglutinin and concanavalin A, were suppressed in spleen-cell cultures of progressors. Passage of spleen cells from progressors over rayon adherence columns or pretreatment with an iron/magnet technique resulted in almost complete restoration of MLTI and mitogen responses. Addition of spleen cells from progressors depressed the MLTI of spleen cells from regressors and the mitogen reactivity of normal spleen cells. Serum from progressors also suppressed MLTI and mitogen reactivity. These data indicate that, in spleens of rats bearing progressively growing tumors, suppressor cells can be demonstrated which inhibit specific reactivity to tumor-associated antigens and non-specific reactivity to mitogens. The presence of suppressor cells or of inhibitory factors in the serum may contribute to the immunosuppression frequently observed in tumor-bearing hosts.
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PMID:Inhibition of in vitro lymphoproliferative responses to tumor-associated antigens by suppressor cells from rats bearing progressively growing Gross leukemia virus-induced tumors. 117

The conditions for generation of simultaneous and independent cytotoxic lymphocyte (CL) responses to each of two sets of alloantigens of limited cross-reactivity by mouse spleen cells in vitro have been investigated. Responder spleen cells were incubated with mitomycin C-treated C57BL/6 (H-2b) or DBA/2 (H-2d) stimulator spleen cells and day 5 CL responses were assayed with 51Cr-labeled EL-4 leukemia (H-2b) and P815 mastocytoma (H-2d) as target cells. Spleen cells from mice of the various H-2 haplotypes tested differed greatly in their ability to develop specific CL responses against alloantigens on the stimulator spleen cells and in the degree of cross-reactive cytotoxic activity against target cells bearing alloantigens not present on the stimulator spleen cells. In contrast to the other strains examined, DBA/1 (H-2q) spleen cells developed specific CL responses to either H-2b or H-2d alloantigens without exhibiting significant cross-reactive activity on the inappropriate target cell. The CL responses to H-2b and H-2d alloantigens by DBA/1 spleen cells were comparable in magnitude and had similar stimulator cell-dose requirements. Further, DBA/1 spleen cells developed CL responses of normal magnitude simultaneously against both target cells when incubated with both mitomycin C-treated C57BL/6 and DBA/2 stimulator cells.
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PMID:Cell-mediated immune responses in vitro. II. Simultaneous generation of cytotoxic lymphocyte responses to two sets of alloantigens of limited cross-reactivity. 118 65

The proliferative activity of bone marrow from Rauscher Leukemia Virus infected mice was studied during the course of the disease. Spleen colony assay and thin-layer agar technique, both presumably reflecting the number of pluripotent hemopoietic stem cells, showed a 2.6 times increase in colony forming units (CFU-S resp. CFU-A) at 12 days after infection. The Bradley method of culturing colonies in agar, which is stated to reflect the number of myeloid precursor cells, resulted in a slower rise in colony forming units (CFU-C) with a maximum of 2.3 times increase at 19 days after infection. These results were compared to the differentiation patterns of the bone marrow at similar intervals after infection. The course of the CFU-C curve parallelled the rise in the number of the myeloblasts in the bone marrow. The pattern of CFU-A and CFU-S curves preceded the rise in number of CFU-C by 7 days. It was found, that RLV infection apart from causing an erythroblastosis in the spleen and a severe anemia is followed by a disappearance of neutrophil granulocytes from the bone marrow. The latter phenomenon is probably the primary cause of the increase of hemopoietic stem cells.
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PMID:The relation between the proliferative activity and the differentiation pattern of bone marrow cells from Rauscher leukemia virus infected BALB/c mice. 122 10


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