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

The ability of partially purified human and guinea-pig haematogenous cell populations, when cultured in vitro, to metabolise arachidonic acid (AA) has been studied. Supernatants from 24 hour cell culture have been subjected to analysis for products of AA metabolism by gas chromatography with electron-capture detection. The cell types studied were human peripheral blood monocytes (both glass adherent and non-adherent), neutrophils, eosinophils and leukemia leucocytes; thoracic duct lymphocytes and lung alveolar macrophages. From the guinea-pig, induced and non-induced macrophage or neutrophil enriched peritoneal exudate populations, lymph node cells, peritoneal eosinophils and peripheral blood platelets were examined. Supernatants were assayed for the presence of PGE2, PGD2, PGF2 alpha, TXB2 and 6-keto-PGF1 alpha. In all types studied PGE2 and TXB2 were the major products formed. The identification of PGE2 and TXB2 was confirmed by GC/MS with multiple ion monitoring. The results have been compared with other reports and their possible significance discussed in relation to the proposed role of prostaglandins as mediators and modulators in immunopathology.
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PMID:Prostaglandin and thromboxane production by human and guinea-pig macrophages and leucocytes. 49 59

Interferons have been demonstrated by animal experimentation to have antiviral, antitumoral and immune effects. Clinical trials of human recombinant alpha-interferon have shown a substantial therapeutic effect in various chronic leukemias and lymphomas. Studies concerning the mechanisms of the anti-leukemia effect of the various interferons have demonstrated that they play an important role in regulating the proliferation of normal and leukemic cells. These lymphokines interact with other important biological mediators such as interleukins, growth factors, factors associated with angiogenesis, etc. New therapeutic developments in oncology and in immunopathology may be expected in the near future.
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PMID:[Human interferons: biological and clinical promises and premises]. 170 21

The human lymphocytotropic retroviruses, despite the fact that their immunopathology varies from acute immunodeficiency to leukemia, have several features in common: they are exogenous viruses isolated from mature T cells, especially T4+ T-cells; they preferentially infect mature T4+ T cells in vitro, although other kinds of cells can be infected (no pathologic effects have been associated with infection of nonlymphoid cells); they possess a reverse transcriptase with similar size and preference for Mg++; they have a unique pX sequence in their genome which codes for a protein which is responsible for trans-activation of viral and possibly cellular genes, and in vitro infection of some T cells induces either continuous proliferation or cytotoxicity which mimic the in vivo manifestations of the virus.
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PMID:Immunopathology associated with human lymphotropic retroviruses. 242 86

The tissue damage caused by virus infection has been traditionally explained by the ability of viruses to multiply in cells and thereby injure or destroy them. Recent evidence suggests, however, that lesions may also be caused by the host's immune response to viral antigens and that the immune system itself may be perturbed by some viruses. This memorandum reviews recent developments in viral immunopathology, with special reference to animal model systems, and indicates the possible relevance of the new concepts and techniques for certain diseases of man. Certain viruses, notably the leukaemia viruses and some of those causing persistent infections, depress the host's ability to mount an antibody response to antigens, while other viruses may enhance the antibody response. Cell-mediated immunity may also be depressed. Another immunopathological manifestation of virus infection is immune-complex disease. When viruses or their antigens persist in the circulation they combine with specific antibody, and the resulting complexes lodge in various sites, especially the kidney. Further combination with complement leads to the release of tissue-damaging substances. A third condition associated with virus infection is antibody-mediated immunologic injury. Both oncogenic and non-oncogenic viruses frequently induce new antigens on the surface of the cells they invade. When antibody attaches to these antigens in the presence of complement, the cells are destroyed.
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PMID:Virus-associated immunopathology: animal models and implications for human disease. 1. Effects of viruses on the immune system, immune-complex diseases, and antibody-mediated immunologic injury. 440 92

A series of Thy-1.2+ Ly-1+ Qa-1+ malignant T cell clones have been isolated from murine sarcoma virus-murine leukemia-Moloney (MSV-MuLV-M)-induced B cell lymphomas or from MSV-MuLV-M-infected B6 mice. These T cell clones enhance both antigen-independent and -dependent lymphocyte differentiation and function. They also induce the differentiation of granulocytes and erythrocytes in the stem cell compartment, a function that parallels the immunopathology of the disease in vivo. The malignant T cell appears to sustain B lymphoma growth in vivo by releasing a factor (BCGF) that promotes B cell proliferation.
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PMID:Regulation of B cell lymphomagenesis by a malignant Qal+ inducer T cell clone. 632 29

This paper describes a method for processing fresh tissue that allows immunohistological analysis on paraffin sections. The method is based on the use of periodate-lysine-paraformaldehyde fixation. The effects of variation in fixation time, concentration of paraformaldehyde, dehydration, clearing, wax embedding and enzyme treatment of cut sections were examined. An optimal processing procedure was established that retains good tissue morphology and allowed 21 out of 27 monoclonal antibodies tested to be used successfully on paraffin sections to identify all major cell subpopulations by their membrane antigenic characteristics. The value of this approach in studying the immunopathology of potentially dangerous infectious diseases and in leukaemia/lymphoma diagnosis is discussed.
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PMID:The demonstration of cell surface antigens on T cells, B cells and accessory cells in paraffin-embedded human tissues. 639 50

Murine acquired immunodeficiency syndrome (MAIDS) is a complex immunopathology caused by a defective murine leukemia virus (LP-BM5) that mainly targets B-lymphocytes. Lymphadenophathy, splenomegaly, hypergammaglobulinemia and progressive immunodeficiency are prominent features of MAIDS. Previously, we showed that the ubiquitin proteolytic system was upregulated in infected lymph nodes [Crinelli, R., Fraternale, A., Casabianca, A. & Magnani, M. (1997) Eur. J. Biochem. 247, 91-97]. In this report, we demonstrate that increased 26S proteasome activity is responsible for accelerated turnover of the IkappaBalpha inhibitor in lymph node extracts derived from animals with MAIDS. The molecular mechanisms mediating IkappaBalpha proteolysis involved constitutive phosphorylation of IkappaBalpha at Ser32 and Ser36 and subsequent ubiquitination, suggesting persistent activation of an NF-kappaB inducing pathway. Interestingly, enhanced IkappaBalpha degradation did not result in enhanced NF-kappaB DNA binding activity, but rather in a different subunit composition. The modulation of NF-kappaB/IkappaB system may affect multiple immunoregulatory pathways and may in part explain the mechanisms leading to the profound immune dysregulation involved in MAIDS pathogenesis.
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PMID:Activation of the ubiquitin proteolytic system in murine acquired immunodeficiency syndrome affects IkappaBalpha turnover. 1042 5

The expression of Fas-Ligand (Fas-L) on microglia could be relevant in multiple sclerosis immunopathology. The present study was performed to evaluate in vitro the expression of Fas-L in human microglial cells both unstimulated and after stimulation with IFN-gamma, beta-IFN-1b and beta-IFN-1b+IFN-gamma. Cells were stimulated for 6,12, 24 and 48 h. Surface Fas-L was evaluated by flow cytometry, total Fas-L by Western blot, whereas mRNA for Fas-L was measured by RT-PCR. We also evaluated the capacity of microglial cells to induce, in vitro, apoptosis on Fas-positive T leukemia Jurkat cells. Our results showed a constitutive expression of Fas-L on microglia. IFN-gamma downregulated the expression of the molecule, while beta-IFN-1b and beta-IFN-1b+IFN- gamma did not. The amount of surface Fas-L was related to the ability of microglial cells to induce apoptosis in Fas-positive target cells, which was partly inhibited by blockade of the Fas-Fas-L pathway.
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PMID:Modulation of fas-ligand (Fas-L) on human microglial cells: an in vitro study. 1074 51

Brain levels of TNF-alpha increase in many inflammatory conditions, including HIV-1 infection, and may contribute to neurodegenerative processes. The paucity of agents that can selectively and potently block TNF-alpha processing or its receptors has led us to investigate the role of TNF-alpha in chronic neurodegeneration associated with retroviral infection using mice with targeted deletions of the TNF-alpha gene. Infection of wild-type C57BL/6 mice with the LP-BM5 murine leukemia retrovirus mixture leads to the development of a severe immunodeficiency as well as cognitive deficits and neuronal damage. TNF-alpha-(-/-) mice infected with LP-BM5 developed a systemic immunopathology indistinguishable in severity from that observed in contemporaneously infected wild-type mice. In contrast, the performance of infected TNF-alpha-(-/-) mice in the Y-maze and Morris water maze was not different from that of uninfected TNF-alpha-(-/-) mice. The extent of glial activation in the striatum, as indicated by the increase in density of peripheral benzodiazepine receptors, was equivalent in both groups of LP-BM5-infected mice. However, the decrease in striatal MAP-2 expression, a marker of neurodegeneration observed in infected wild-type mice, was not found in infected TNF-alpha-(-/-) mice. While the loss of TNF-alpha appeared to have no effect on the course or severity of the central or peripheral immunopathology resulting from LP-BM5 infection, the behavioral and biochemical manifestations were substantially curtailed in the TNF-alpha-(-/-) mice. These findings directly support a role for TNF-alpha in the neurodegenerative processes associated with viral infections such as HIV-1.
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PMID:Suppression of neurocognitive damage in LP-BM5-infected mice with a targeted deletion of the TNF-alpha gene. 1078 58

A great number of authors consider as "stem cell disorders" the following immunopathologies: immunodeficiency, lymphoproliferative diseases, systemic and organ-specific autoimmune diseases. A participation of early hemopoietic precursors in immunopathology development was analyzed on the next models: age-related immunodeficiency in CBF1 mice, autoimmune hemolytic anemia in NZB mice and leukemia in AKR mice. NZB mice have an augmented number of CFUs in S-phase, as a prerequisit for elevated sensitivity to Rauscher leukemia virus, as well to autoimmune disorder development. The increased stem cell proliferation (45% of CFUs in S-phase) in AKR mice is accompanied by changes in CFU redistribution: a decrease of CFU number in bone marrow and their increase in spleen. The hallmark of "disregulation" in bone marrow of old mice is the augmentation of erythroid precursors and the decrease in the number of myeloid precursors (GM-CFU and M-CFU), in other words the shift of differentiation to erythropoiesis. The augmentation of stem cell proliferation is accompanied by the increase in the number of erythroid precursors to the detriment of myeloid precursors. Therefore, the disturbances in the regulation of proliferation and differentiation of CFUs may contribute to the formation of the immunopathologies. The correction of HSC proliferation and differentiation may be one of the important approaches to the treatment of immune disorders.
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PMID:The Interaction of Hemopoiesis and Immunogenesis in Immunopathology Development. 1268 17


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