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)

Two therapeutic modalities, zidovudine (targeting retroviral replication) and cyclosporin A (targeting immunopathologic consequences of retroviral expression) were evaluated in a murine model of AIDS. In previous studies, cyclosporin A treatment (40 or 60 mg/kg/day) before and after infection with LP-BM5 murine leukemia viruses protected against the development of immunodeficiency disease. The present study extends these findings. First, a low dose of cyclosporin A (20 mg/kg/day) was ineffective, and treatment initiated 5 days after infection did not protect against virus-induced lymphoproliferation and hypergammaglobulinemia. Second, zidovudine added to drinking water (0.1 mg initiated 5 days after infection and continued for 8 weeks) was more effective than 0.2 mg/mL given day 5-12 after infection. This treatment reduced lymph node size, disease severity as determined histologically, retrovirus-induced gp70 expression, and IgE (but not IgM and IgG) levels. Third, combined treatment had an additive, protective effect on lymphocyte proliferative capacity. This successful dual therapeutic strategy in a mouse model has potential applicability for similar approaches in treating human immunodeficiency virus infection.
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PMID:Effect of cyclosporin A and zidovudine on immune abnormalities observed in the murine acquired immunodeficiency syndrome. 163

A 36-year-old man presented with an acute immune-mediated illness characterized by leukocytoclastic vasculitis and polyarthritis. Evaluation of the synovial fluid, bone marrow, and peripheral blood revealed large numbers of abnormal lymphoid cells labeling a 4B4-positive, CD4-positive, IL-2 receptor-negative, helper T cells. Hypergammaglobulinemia, immune complexes, high levels of serum IL-2 receptors, serum antibodies against foreign alloantigens, and specific cytolysis of the patient's leukemic cells by his normal CD8+ T lymphocytes suggest an interaction of the malignant cells and his normal immune cells. Thus, some of the rheumatologic symptoms leading to the diagnosis of leukemia appear to reflect an immunoregulatory imbalance manifested by B-cell hyperactivity, likely induced by the malignant helper T cells, and attempted regulation of his malignant T cells by normal lymphocytes.
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PMID:T helper-cell leukemia/lymphoma: presentation as an acute immune-mediated illness. 213 65

A syndrome characterized by lymphadenopathy, hypergammaglobulinemia, and immunodeficiency develops in C57BL/6 mice inoculated with LP-BM5 murine leukemia viruses. By studying the number and antigenic specificity of B cells activated in the course of this disease, we found that a series of reproducible changes in the humoral immune system were induced by retroviral infection. The rate of B cell proliferation and the proportion of B cells activated to secrete Ig increased by nearly 10-fold at 4 wk post inoculation. B cells producing antibodies reactive with a panel of three conventional Ag and five autoantigens were stimulated simultaneously and proportionally to secrete, demonstrating that such activation was polyclonal in nature. At 12 wk post infection, the number of Ig-secreting B cells continued to rise and significant hypergammaglobulinemia developed. At 16 wk post infection, immunostimulation gave way to immunosuppression, as evidenced by a slight decline in the number of Ig-secreting lymphocytes and a sharp reduction in the concentration of serum antibody. At this time, the B cell repertoires of infected mice diverged markedly from those of uninfected animals. These changes are comparable to those found in some patients infected with HIV, and provide a useful model to study the association between retroviral infection and regulatory abnormalities of the humoral immune system.
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PMID:Characteristics of B cell proliferation and activation in murine AIDS. 246 40

Mice infected with LP-BM5 murine leukemia virus develop lymphadenopathy, splenomegaly, hypergammaglobulinemia, and profound immunosuppression associated with enhanced susceptibility to infection. In this study, molecular genetic analyses of spleen and lymph node cells from infected mice showed the early course of disease was associated with polyclonal proliferations of both B and T cells but that by 12 wk oligoclonal expansions of B or T cells could be detected. When near death, the mice were killed and almost all exhibited clonally restricted populations of B cells, and continuous cultures of B lineage cells were established from three of 19 mice. Histologically, lymph nodes with polyclonal lymphoproliferative lesions were indistinguishable from nodes with clonally restricted populations of cells. However, aggressive immunoblastic lymphomas of characteristic morphology were seen in nonlymphoid organs, particularly in the brain. The demonstration of terminal B cell lymphomas in murine AIDS extends the similarities between this syndrome and AIDS in humans.
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PMID:Evolution of B cell lineage lymphomas in mice with a retrovirus-induced immunodeficiency syndrome, MAIDS. 283 Mar 34

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

Since the discovery of human T-cell leukemia virus type 1 (HTLV-1) in patients with adult T-cell leukemia/lymphoma (ATLL), malignant neoplasms of mature (peripheral) T lymphocytes have attracted a great deal of attention. This type of neoplasm is more common in Japan than in Western countries, and may show distinct clinical pictures such as hypergammaglobulinemia, hypercalcemia, etc. T-cell lymphomas are more prone than B-cell lymphomas to become leukemic. Because of a marked intermingling of reactive cells (histiocytes, eosinophils, etc.), the histologic diagnosis of T-cell lymphoma is often difficult. Proliferation pattern and cellular size do not correlate with prognosis as in B-cell lymphoma. Since T-cell lymphomas often manifest with several distinct clinicopathologic settings, their categorization should be based on several parameters, such as the presence or absence of ATLL-associated antigen in serum, histology, phenotype of the neoplastic cell, and clinical features. Since a classification for T-cell lymphomas has not been established, a further multi-disciplinary approach is necessary for a better understanding of this interesting neoplasm.
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PMID:Peripheral T-cell lymphoma. 306 2

The clinical course of 52 cases with eosinophilic fasciitis observed at the Mayo Clinic has been described. Cutaneous changes included pitting edema, peau d'orange, and induration, and may affect virtually any body surface area. In addition, localized morphea was present in 15 cases. Arthritis was observed in 21 patients; 29 patients had flexion contractures and 12 had carpal tunnel syndrome. Associated hematologic diseases were found in five patients; thrombocytopenia in two, myeloproliferative disorder in one, myelomonocytic leukemia in one, and chronic lymphocytic leukemia in one. Peripheral blood eosinophilia was noted in 33 of 52 patients, hypergammaglobulinemia was noted in 17 of 49, and elevated sedimentation rate was noted in 15 of 52. Nonspecific EMG changes were seen in 11 of 15 patients. None had clinical involvement of the kidneys, lungs, or heart. No significant association between any HLA-A, -B, or -DR and eosinophilic fasciitis was seen. Prednisone and hydroxychloroquine seemed equally beneficial in treatment; however, some cases showed spontaneous recovery, making evaluation of therapeutic efficacy difficult. Relapses occurred in some cases.
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PMID:Eosinophilic fasciitis: clinical spectrum and therapeutic response in 52 cases. 323 80

Sera from 23 individuals with Gaucher disease (GD) were analyzed for hypergammaglobulinemia and oligoclonal and monoclonal gammopathies. Serum IgG level was elevated in 15/23 (65%) patients, and a diffuse hypergammaglobulinemia was present in 10/23 (43%) patients. An oligoclonal gammopathy was noted in six patients, and a monoclonal gammopathy in two. Lymphocyte subset analysis was also carried out in eight individuals with GD. Four of five individuals showed increased surface Ig-positive lymphocytes, while 7/7 were positive for either increased CD19- and/or CD20-positive lymphocytes. An eighth patient was found to have a B-cell leukemia. Statistical analysis of kappa and lambda histograms were suggestive of a monoclonal excess. However, restriction enzyme analysis of four individuals with GD and increased B cells failed to show any evidence of Ig gene rearrangements. Serum Ig abnormalities and perhaps B-cell lymphocytosis appear to be common in the GD patient population and are not associated with circulating monoclonal lymphocytes.
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PMID:Polyclonal B-cell lymphocytosis and hypergammaglobulinemia in patients with Gaucher disease. 326 98

Clinical, hematologic, and immunologic findings for 14 dogs with Ehrlichia canis monoclonal gammopathy were studied retrospectively. Epistaxis, anemia, thrombocytopenia, hypoalbuminemia, hypergammaglobulinemia, and proteinuria were documented in the majority of these dogs. The serum protein electrophoresis pattern was characterized by a distinct narrow-base monoclonal spike, by a broad-base monoclonal spike, or by a monoclonal spike superimposed on a polyclonal gammopathy. The monoclonal spike disappeared following tetracycline treatment for ehrlichiosis. The long-term prognosis following treatment was generally good. The diagnostic features of monoclonal gammopathy due to myeloma were compared with those of E. canis monoclonal gammopathy. Owing to numerous similarities in clinical, hematologic, and immunologic findings, we conclude that an E. canis antibody titer should be determined in all dogs in which a diagnosis of benign monoclonal gammopathy is contemplated or definitive evidence of myeloma, leukemia, or macroglobulinemia is lacking.
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PMID:Monoclonal gammopathy associated with naturally occurring canine ehrlichiosis. 350 17

Serum levels, urinary excretion, and clearances of several proteins of different molecular weights were studied in 18 patients with mono- and myelomonocytic leukemia. Nine patients had normal renal function (group A) and nine had impaired renal function with azotemia (group B). The majority of patients in both groups had increased concentration of immunoglobulins, particularly IgG, IgA, and IgM; IgD level was normal. Serum transferrin and alpha(2)-macroglobulin were frequently reduced while the level of ceruloplasmin was often increased, especially in patients with azotemia. The activity of lysozyme in the serum was high in all patients, but was considerably higher in group B. Proteinuria was found in most patients but was more prominent in group B. Almost invariably albumin constituted less than 25% of the total protein excreted. Qualitative analysis of various urinary proteins by immunochemical techniques and clearance studies suggested the presence of glomerular as well as tubular dysfunction. Determination of urinary lysozyme frequently showed no direct correlation between the serum level of the enzyme and its concentration in the urine or its clearance by the kidney. In addition to glomerular filtration, impaired tubular reabsorption may account for the high level of lysozyme in the urine. It is postulated that the very high level of lysozyme in the glomerular filtrate and possibly hypergammaglobulinemia may play a role in the induction of tubular damage. Renal impairment has been correlated with histological changes in the kidneys. From a comparative study of various leukemias, it seems that the combined glomerular-tubular dysfunction is a manifestation unique to mono- and myelomonocytic leukemia.
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PMID:Serum and urinary proteins, lysozyme (muramidase), and renal dysfunction in mono- and myelomonocytic leukemia. 527 Sep 14


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