Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. In order to investigate exercise-induced changes of beta 2-adrenoceptors on human leukocyte subsets, beta-adrenoceptor density was determined as specific binding of [125I]-iodocyanopindolol to granulocytes, monocytes, B and T lymphocytes of six subjects immediately before and after exercise and after 30 min of rest. 2. A 10 min graded bicycle exercise with a workload of 50-250 W caused a transient increase of granulocytes, monocytes, B and T cells of about 32, 43, 120 and 25%, respectively. 3. While the number of beta 2-adrenoceptors in granulocytes remained unchanged, beta-adrenoceptor densities in B cells, T cells and monocytes increased from pre-exercise mean values of 2730, 870 and 2400 binding sites/cell to 3500, 1230 and 3220 binding sites/cell, respectively, under physical stress. The rise in receptor numbers was accompanied by an enhanced isoprenaline-stimulated cyclic AMP formation in unfractionated mononuclear leukocytes (MNL) of about 26% as well as by a 2-3-fold increase in plasma catecholamine levels. Cell concentrations, beta 2-adrenoceptor numbers and adrenergic responsiveness returned to normal after 30 min rest. 4. Administration of 60 mg prednisone 2 h before exercise resulted in granulocytosis and lymphopenia with a preponderant effect on the exercise-induced rise in B cells and monocytes. Corticosteroids showed no effect on stress-induced changes of beta 2-adrenoceptors and responsiveness. 5. It is concluded that exercise-induced increases in beta 2-adrenoceptor density and adrenergic responsiveness of unfractionated MNL are caused by a release of receptor-enriched cells into the circulation, particularly of B lymphocytes and monocytes which carry the highest beta 2-adrenoceptor density.
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PMID:Alterations of beta-adrenoceptors on human leukocyte subsets induced by dynamic exercise: effect of prednisone. 285 48

The adenosine deaminase, 5'-nucleotidase, AMP-aminohydrolase and adenylate kinase activities and thymostimulin influence on these indices in vivo were studied in rat thymus and spleen lymphocytes in the latent period of DMBA-induced mammary carcinogenesis. The adenosine deaminase activity was established to increase while 5'-nucleotidase and AMF-aminohydrolase activity to decrease in the thymocytes of intact animals treated with thymostimulin; the adenylae kinase activity of spleen lymphocytes decreased as compared with that in the rats not treated with the preparation. The dynamics of changes in the investigated enzymes in activities in lymphocytes was of wave-like pattern in the latent period. The treatment of animals with thymostimulin in this period normalized adenosine deaminase activity and decreased the activity of the other enzymes in these cells.
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PMID:[Influence of thymostimulin on the activity of certain enzymes of adenosine and AMP metabolism in lymphocytes of rats with mammary cancer]. 628 53

Transient granulocytopenia and lymphopenia may occur in acute alcoholics without splenomegaly, cirrhosis, infection, and megaloblastic anemia due to folate deficiency. The bone marrow in granulocytopenic patients is frequently hypocellular with few mature granulocytes, and the functional marrow granulocyte reserve is reduced. These findings suggest a depressed granulopoietic activity in these patients. The mechanism by which alcohol suppresses granulopoiesis remains unclear. Direct toxicity of alcohol on granulopoietic stem cells and increased individual susceptibility to the toxic effect of alcohol may be important factors. Alcohol also causes functional impairment of granulocytes (adherence, motility, and chemotaxis), macrophages (motility and phagocytosis), and lymphocytes (blastogenic transformation and development of delayed dermal hypersensitivity reaction), probably by perturbation of the cell membrane resulting in an increased intracellular cyclic AMP level.
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PMID:Effects of alcohol on granulocytes and lymphocytes. 737 52

1. CD19+ B lymphocytes were purified from the peripheral blood of normal and atopic subjects to analyse and compare the phosphodiesterase (PDE) activity profile, PDE mRNA expression and the importance of PDE activity for the regulation of B cell function. 2. The majority of cyclic AMP hydrolyzing activity of human B cells was cytosolic PDE4, followed by cytosolic PDE7-like activity; marginal PDE3 activity was found only in the particulate B cell fraction. PDE1, PDE2 and PDE5 activities were not detected. 3. By cDNA-PCR analysis mRNA of the PDE4 subtypes A, B (splice variant PDE4B2) and D were detected. In addition, a weak signal for PDE3A was found. 4. No differences in PDE activities or mRNA expression of PDE subtypes were found in B cells from either normal or atopic subjects. 5. Stimulation of B lymphocytes with the polyclonal stimulus lipopolysaccharide (LPS) induced a proliferative response in a time- and concentration-dependent manner, which was increased in the presence of interleukin-4 (IL-4). PDE4 inhibitors (rolipram, piclamilast) led to an increase in the cellular cyclic AMP concentration and to an augmentation of proliferation, whereas a PDE3 inhibitor (motapizone) was ineffective, which is in accordance with the PDE profile found. The proliferation enhancing effect of the PDE4 inhibitors was partly mimicked by the cyclic AMP analogues dibutyryl (db) cyclic AMP and 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole-3',5'-cyclic monophosphorothioate, Sp-isomer (dcl-cBIMPS), respectively. However, at concentrations exceeding 100 microM db-cyclic AMP suppressed B lymphocyte proliferation, probably as a result of cytotoxicity. Prostaglandin E2 (PGE2, 1 microM) and forskolin (10 microM) did not affect B cell proliferation, even when given in combination with rolipram. 6. Inhibition of protein kinase A (PKA) by differentially acting selective inhibitors (KT 5720, Rp-8-Br-cyclic AMPS) decreased the proliferative response of control cells and reversed the proliferation enhancing effects of rolipram. 7. Importantly, PDE4 activity in LPS/IL-4-activated B lymphocytes decreased by about 50% compared to unstimulated control values. 8. We conclude that an increase in cyclic AMP, mediated by down-regulation of PDE4 activity, is involved in the stimulation of B cell proliferation in response to LPS/IL-4. B cell proliferation in response to a mitogenic stimulus can be further enhanced by pharmacological elevation of cyclic AMP.
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PMID:Phosphodiesterase profile of human B lymphocytes from normal and atopic donors and the effects of PDE inhibition on B cell proliferation. 955 83

Reticular dysgenesis is a human severe combined immunodeficiency that is primarily characterized by profound neutropenia and lymphopenia. The condition is caused by mutations in the adenylate kinase 2 (AK2) gene, resulting in the loss of mitochondrial AK2 protein expression. AK2 regulates the homeostasis of mitochondrial adenine nucleotides (ADP, ATP and AMP) by catalyzing the transfer of high-energy phosphate. Our present results demonstrate that AK2-knocked-down progenitor cells have poor proliferative and survival capacities and are blocked in their differentiation toward lymphoid and granulocyte lineages. We also observed that AK2 deficiency impaired mitochondrial function in general and oxidative phosphorylation in particular - showing that AK2 is critical in the control of energy metabolism. Loss of AK2 disrupts this regulation and leads to a profound block in lymphoid and myeloid cell differentiation.
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PMID:AK2 deficiency compromises the mitochondrial energy metabolism required for differentiation of human neutrophil and lymphoid lineages. 2627 Mar 50

Objective We elucidated the effectiveness of a humanized CCR4 antibody (mogamulizumab) on adult T-cell leukemia-lymphoma (ATL), which typically has a poor outcome. Methods We retrospectively analyzed 14 patients with aggressive ATL who had been treated at our institution with weekly cycles of mogamulizumab for eight weeks from 2012-2014. Results The patients (median age: 63 years old) were classified as having acute- (n=10) or lymphoma-type (n=4) ATL. The prior treatment regimens consisted of CHOP, VCAP-AMP-VECP, DeVIC and CHASE, with an average of two courses (range: 1-4). The prior disease responses were partial remission (n=3) and progressive disease (n=11). The treatment was administered in the primary refractory setting (n=8), for relapse (n=2), or as bridging therapy before hematopoietic stem cell transplantation (n=4). The overall response rates were 64% and 43% after four and eight cycles (or after the final cycles), respectively. The median overall survival (OS), OS rate at six months and OS rate at 12 months were 66 days, 41.7% and 20.8%, respectively. All of the patients with acute-type ATL who showed a response to treatment had an early response. Notably, six of the 14 ATL patients showed somewhat prolonged survival (>100 days). However, relapse or disease progression in the peripheral blood, central nervous system, lymph nodes, skin, and/or bone occurred within a relatively short period after treatment. The adverse effects were tolerable, and included lymphopenia, cytomegalovirus infection and skin rash. Conclusion Mogamulizumab therapy resulted in an early and high remission rate and somewhat prolonged survival in patients with refractory ATL. However, the duration of remission was short, and there was early relapse and disease progression. This study may show the current impact of mogamulizumab in clinical practice.
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PMID:Clinical Impact of a Humanized CCR4 Antibody (Mogamulizumab) in 14 Patients with Aggressive Adult T-cell Leukemia-lymphoma Treated at a Single Institution During a Three-year Period (2012-2014). 2725 49