Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most sera from leukaemic cattle inhibited phagocytic activity of normal bovine peripheral polymorphonuclear leukocytes, growth of interleukin 2-dependent bovine T cells and mitogen-induced (phytohaemagglutinin, concanavalin A, pokeweed mitogen, lipopolysaccharide and protein A) blastogenesis of normal bovine lymphocytes. By contrast, antibody-dependent, and spontaneous cell-mediated cytotoxicity were suppressed by only a few sera. The antibody titer against bovine leukaemia virus in these sera correlated with the percent inhibition of lymphocyte blastogenesis. These leukotic sera had no direct cellular cytotoxicity and the inhibitory activity was not lost by dialysis or heat inactivation at 62 degrees C for 30 min. However, the activity was reduced by heating at 80 degrees C for 30 min. Neither the concanavalin A sepharose 4B effluent fraction nor 3.5% polyethyleneglycol-treated serum was found to contain significant lymphocyte-inhibitory activity. Blastogenic transformation of lymphocytes prepared from leukaemic cattle was hardly detectable; however, the mitogen responsiveness of these lymphocytes was improved by a 37 degrees C 1-h preincubation followed by washing.
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PMID:Inhibition of in vitro immunocyte function by sera from cattle with bovine leukosis. 284 33

The T lymphocyte-derived lymphokine interleukin 2 and the cell-associated receptor for this molecule play major roles in the activation and regulation of the human immune response. An enzyme-linked immunosorbent assay has been developed to measure quantitatively a soluble form of one component of the human interleukin 2 receptor, namely the Tac peptide. In the present studies, soluble Tac peptide was measured in the urine of normal individuals (mean = 92 U/ml), a level not significantly different (0.01 less than P less than 0.05) from the corresponding serum concentrations (mean = 175). The urinary Tac peptide had a molecular weight of 40-45 kD by sodium dodecyl sulphate-polyacrylamide gel electrophoresis analysis and specifically bound interleukin 2. Elevated levels of urinary Tac peptide were found in four patients with adult T cell leukaemia who also had elevated serum levels of Tac peptide. Thus, urine may represent a valuable source of lymphokine-binding proteins that may serve as important markers of immunological activation.
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PMID:Soluble Tac peptide is present in the urine of normal individuals and at elevated levels in patients with adult T cell leukaemia (ATL). 284 56

Cats exposed to the feline leukemia virus (FeLV) may mount an effective immune response and eliminate the virus, develop a non-viremic, latent infection or become persistently infected and shed the virus. Persistently infected cats commonly die of secondary opportunistic infections that result from FeLV-induced immunosuppression. The acquired immunosuppression is the most frequent and most devastating consequence of FeLV infection in the cat. Immunosuppression is targeted primarily to the cell-mediated immune system and has been attributed to the viral p15e envelope protein. The decreased IgG response and proliferative response to T cell mitogens is thought to be due to a defect in the helper cell function. As a result of T helper cell immunosuppression, infected cats may also have defective cytotoxic lymphocyte and activated macrophage functions which are regulated by their lymphokines. Research has shown that the virus causes a general suppression in the production of T cell-derived lymphokines, including gamma interferon and interleukin 2. A decrease in the function of polymorphonuclear leukocytes has also been reported and may contribute to deaths due to opportunistic infections in FeLV-positive cats. There are numerous parallels between the acquired immunodeficiency syndrome (AIDS) in man and the FeLV-induced immunodeficiency syndrome in cats. Frequent deaths due to opportunistic infections, lymphopenia, depressed cell-mediated immune responses to T cell-dependent antigens despite hypergammaglobulinemia and the presence of a long period of time between infection and the onset of clinical signs are just a few of the syndromes that are similar between the 2 retroviral diseases. A new strain of FeLV, FeLV-FAIDS has been associated with a naturally occurring immunosuppressive syndrome that is strikingly similar to AIDS in man. In addition, a T-lymphotropic retrovirus has recently been identified from cats with an immunodeficiency-like syndrome; this feline lentivirus disease is morphologically similar, but antigenically distinct from the human immunodeficiency virus, the cause of AIDS. Treatment for FeLV immunosuppression is primarily supportive. The development of a soluble tumor cell antigen vaccine has been shown to be efficacious in preventing FeLV infections.
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PMID:Clinical and immunologic aspects of FeLV-induced immunosuppression. 284 93

The effects of calcium, calcium antagonists, and calmodulin inhibitors on the growth of adult T-cell leukemia (ATL) cells were studied in vitro. Fresh ATL cells from patients and established ATL cell lines did not grow well in a low-calcium (less than 0.01 mM) medium. However, their growth was enhanced by the addition of calcium to the medium in a dose-dependent manner. The maximum response was induced at 4 mM calcium, which was higher than that of the normal serum calcium level, 2.5 mM. Other leukemia cells, except ATL, grew well in the low-calcium medium, and their growth was not enhanced by the addition of calcium. Calcium antagonists and calmodulin inhibitors inhibited the growth of ATL cells at the concentration of 10(-5)-10(-7) M, while they did not inhibit the growth of other leukemia cells. Furthermore, the expression of interleukin 2 receptors (Tac antigens) on ATL cells was also enhanced by calcium and was inhibited by calcium antagonists and calmodulin inhibitors. In accordance with these results, the increase of the extracellular calcium concentration resulted in the increase of the intracellular calcium concentration in ATL cells, but not in other leukemia cells. These results suggest that calcium and calmodulin play a critical role in regulating the growth of ATL cells.
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PMID:Calcium dependency in the growth of adult T-cell leukemia cells in vitro. 286 35

The mechanism of immunodeficiency in adult T-cell leukemia (ATL) patients was studied in vitro. Peripheral blood lymphocytes from ATL patients and ATL cell lines such as Hut 102, MT 1, and MT 2 were not activated to proliferate by the stimulation with concanavalin A and suppressed normal lymphocyte proliferative responses induced with concanavalin A when cultured together. The sera from ATL patients and the culture supernatants from ATL cells and ATL cell lines also suppressed normal lymphocyte proliferative responses induced with concanavalin A. By Sephacryl S-200 column chromatography, the suppressive factors were fractionated as a single peak with the molecular weights of 50,000 to 70,000. The suppressive factors were unstable to acid treatment but stable to the treatment with base, heat, freezing-thawing, and trypsin. The factors suppressed the production of interleukin 2 by T-cells and the responsiveness of T-cells to interleukin 2, but not the expression of interleukin 2 receptors on T-cells and the production of interleukin 1 by monocytes. These results suggest that the immunosuppressive factors produced by ATL cells have some roles in the induction of immunodeficient states in ATL patients.
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PMID:Immunosuppressive factors from adult T-cell leukemia cells. 287 86

The adult T cell leukemia (ATL) is a T cell neoplasm etiologically associated with human T lymphotropic virus type I (HTLV-I) infection. ATL cells often abnormally express interleukin 2 (IL-2) receptors, and ATL patients may show clinical evidence of hypercalcemia, osteolytic bone lesions, or increased bone turnover. Whereas interleukin 1 (IL-1) is not generally recognized as a product of T cells, this cytokine is capable of both altering IL-2 receptor expression and activating osteoclasts. Thus, we investigated the possibility that primary ATL leukemic T cells and HTLV-I-infected long-term ATL cell lines produce IL-1. S1 nuclease protection assays demonstrated that primary leukemic ATL cells from five out of six patients, as well as one patient with T4+ chronic lymphocytic leukemia, contained considerable quantities of IL-1 beta messenger RNA (mRNA) and small amounts of IL-1 alpha mRNA. These primary leukemic T cells also released biologically active IL-1 protein as evaluated in the murine thymocyte comitogenesis bioassay. In contrast to primary tumor cells, four out of six long-term ATL cell lines produced variable amounts of IL-1 alpha mRNA in the absence of detectable IL-1 beta mRNA as measured by S1 nuclease protection. These data demonstrate that IL-1 gene (especially IL-1 beta) expression occurs in many primary HTLV-I-infected leukemic T cells raising the possibility that this mediator may play a role in the pathological changes associated with this leukemia. Also, these studies show that the pattern of IL-1 alpha and IL-1 beta gene expression differs between primary ATL tumor cells and long-term cultured ATL cell lines, indicating an interesting biological difference in these two HTLV-I-infected cell populations.
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PMID:Interleukin 1 gene expression in adult T cell leukemia. 288 87

Human T cell leukemia/lymphoma (T-lymphotropic) virus type I (HTLV-I) infection has been considered to be closely associated with the leukemogenesis of adult T cell leukemia (ATL), in which interleukin 2 (IL-2) receptors are abnormally expressed. In this study, however, Southern blot analysis revealed no gross rearrangement or obvious amplification of the IL-2 receptor gene in ATL leukemic cells, indicating that abnormal IL-2 receptor expression in ATL is not due to the structural change of its gene. Hence, we studied the expression of the IL-2 receptor and HTLV-I at the RNA level during short-term cultures of leukemic cells from 9 ATL patients. Cytoplasmic dot hybridization and Northern hybridization revealed that fresh leukemic cells from seven of nine patients expressed a small amount of IL-2 receptor mRNA but HTLV-I RNA was undetectable in all cases. After cultures for up to 7 d, both IL-2 receptor mRNA and HTLV-I RNA (including pX message) expression concomitantly increased, whereas the amounts of other cellular genes, except for beta-actin, did not. The increases in their RNA expression were inhibited by early addition (within 12 h after the beginning of the culture) of cycloheximide, indicating that these increases are mediated by newly synthesized protein(s). These results strongly suggested that IL-2 receptor expression is closely associated with HTLV-I expression in leukemic cells from ATL patients.
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PMID:Close association between interleukin 2 receptor mRNA expression and human T cell leukemia/lymphoma virus type I viral RNA expression in short-term cultured leukemic cells from adult T cell leukemia patients. 289 29

Human T-cell lymphotropic virus type 1 (HTLV-I), the etiologic agent of human T-cell leukemia, has recently been shown to be associated with neurologic disorders such as tropical spastic paraparesis, HTLV-associated myelopathy, and possibly with multiple sclerosis. In this communication, we have examined one specific case of neurologic disorder that can be classified as multiple sclerosis or tropical spastic paraparesis. The patient suffering from chronic neurologic disorder was found to contain antibodies to HTLV-I envelope and gag proteins in his serum and cerebrospinal fluid. Lymphocytes from peripheral blood and cerebrospinal fluid of the patient were shown to express viral RNA sequences by in situ hybridization. Southern blot analysis of the patient lymphocyte DNA revealed the presence of HTLV-I-related sequences. Blot-hybridization analysis of the RNA from fresh peripheral lymphocytes stimulated with interleukin 2 revealed the presence of abundant amounts of genomic viral RNA with little or no subgenomic RNA. We have cloned the proviral genome from the DNA of the peripheral lymphocytes and determined its restriction map. This analysis shows that this proviral genome is very similar if not identical to that of the prototype HTLV-I genome.
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PMID:Molecular cloning of human T-cell lymphotrophic virus type I-like proviral genome from the peripheral lymphocyte DNA of a patient with chronic neurologic disorders. 289 23

BALB/c mice fail to mount significant cell-mediated immunity against the syngeneic virally induced leukemia MCDV-12, and die approximately 10 days after tumor inoculation. Our studies in vitro demonstrated that BALB/c splenocyte and irradiated MCDV-12 cell co-culture led to reduced alloreactivity, including depressed interleukin 2 (IL 2) production. Tumor-induced immune suppression was genetically restricted, antigen nonspecific, and alleviated in part by exogenous IL 2 administration in vitro. Furthermore, mitogen stimulation of IL 2 production, not requiring self or alloantigen recognition, was unaffected by MCDV-12 exposure. These results indicate that tumor cells may escape from immunosurveillance by reducing IL 2 production in the immediate tumor vicinity, and suggest a potential role for major histocompatibility complex antigens in the immunosuppression mechanism.
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PMID:Murine leukemic cells inhibit IL 2 production by susceptible syngeneic splenocytes. 293 79

The current studies were designed to evaluate the effectiveness of marrow transplantation within and outside the major histocompatibility complex (MHC) on the long-term survival and occurrence of spontaneous leukemia in AKR mice. AKR mice, which were lethally irradiated and received MHC-matched marrow from CBA/J mice (CBA----AKR), never developed leukemia and were alive and remained healthy for up to 280 days post-transplant. These long-term surviving chimeras possessed substantial immune vigor when both cell-mediated and humoral responses were tested. Lethally irradiated AKR mice, which had received MHC-mismatched marrow (anti-Thy-1.2 treated or nontreated) from C57BL/6J mice (B6----AKR), never developed leukemia and survived up to 170 days post-transplant. However, both groups of these chimeras began dying 180 to 270 days post-transplant due to a disease process which could not be readily identified. Histological analysis of B6----AKR chimeras revealed severe lymphoid cell depletion in thymus and spleen; however, none of these chimeras exhibited classical features of acute graft versus host disease. Concanavalin A mitogenesis, primary antibody responses to sheep red blood cells and the production of interleukin 2 (IL-2) were suppressed in B6----AKR chimeras. IL-2 treatment of B6----AKR chimeras was shown to partially correct these deficiencies without stimulating mixed lymphocyte responsiveness to donor or host lymphocytes. These studies indicate that the use of MHC-mismatched marrow for the prevention of spontaneous AKR leukemia may rely on augmentative IL-2 therapy for complete immune reconstitution of leukemia-free chimeras.
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PMID:Leukemia prevention and long-term survival of AKR mice transplanted with MHC-matched or MHC-mismatched bone marrow. 294 11


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