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)

A longitudinal investigation has been conducted into the cell-mediated immune responses of onchocerciasis patients after a single-dose treatment with ivermectin. Untreated patients tested for delayed cutaneous hypersensitivity (DCH) to seven recall antigens showed lower responses than infection-free control individuals (P less than 0.01), but 6 and 14 months after treatment DCH reactions increased to similar levels to those seen in the controls. The in vitro cellular reactivity to Onchocerca volvulus-derived antigen (OvAg) was reduced in untreated patients as compared with controls, and the lymphocyte blastogenic responses to OvAg and streptolysin-O clearly improved up to 14 months after treatment. Peripheral blood mononuclear cells (PBMC) from untreated patients produced IL-1 beta, tumour necrosis factor-alpha (TNF-alpha) and IL-6 in response to mitogenic stimulation with phytohaemagglutinin (PHA), only low levels of IL-1 beta, IL-2 and TNF-alpha in response to OvAg, but higher amounts of IL-4 and interferon-gamma (IFN-gamma) in response to OvAg than control individuals. After ivermectin treatment, the OvAg-induced production of IL-1 beta and TNF-alpha increased significantly 1 and 14 months after treatment. The PHA-induced production of IL-2 and IL-4 increased 1 month after treatment and remained significantly elevated until 14 months after treatment, whereas the OvAg-specific secretion of IL-2, IL-4 and IFN-gamma did not change after ivermectin treatment. Flow cytometric analysis of lymphocyte-subsets in the peripheral blood of untreated patients revealed a relative and absolute (P less than 0.01) diminution of CD4+ cells and a significantly smaller CD4+/CD8+ cell ratio as compared with controls. By 4 weeks after treatment and thereafter, CD4+ T cells increased relatively and absolutely (P less than 0.01); likewise there was an absolute increase in T-helper-inducer cells (CD4+CD45RO+) and a temporarily improved CD4+/CD8+ cell ratio (P = 0.001). The expression of the low-affinity receptor for IgE (CD23) on total lymphocytes decreased from 14% to 7% by 14 months after treatment. The CD8+ cells and CD3+TCR gamma delta + cells were higher in patients than in controls and both remained elevated until 14 months after treatment. These results suggest a distinctly improved cellular immunity in human onchocerciasis that was facilitated by ivermectin therapy.
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PMID:Ivermectin-facilitated immunity in onchocerciasis. Reversal of lymphocytopenia, cellular anergy and deficient cytokine production after single treatment. 151 57

Flow cytometric analysis was carried out on peripheral blood cells from patients with tuberculosis (TB) (n = 84) and with mycobacteriosis other than tuberculosis (MOTT) (n = 38). A whole blood-staining-hemolysis procedure was used for the preparation of samples being analyzed, and the cells were double-stained with various combinations of fluorescein isothiocyanate (FITC)- and phycoerythrin (PE)- labeled monoclonal antibodies. These procedures enabled us to obtain quite reproducible results. As patients of more than 70 years old showed apparently distinct T lymphocyte profiles compared with those less than 70 years of age, this investigation was carried out only on patients of less than 70 years old. 1) The proportion of total lymphocytes to total leukocytes was significantly low in TB- and MOTT- groups, when compared with that in the healthy control group, although the total peripheral leukocyte number was not significantly different from each other. Thus, absolute numbers of lymphocytes were decreased significantly in TB- and MOTT- patients. 2) The numbers of both T and B lymphocytes in peripheral blood decreased in patients of both groups, leaving the ratio of T/B relatively constant. 3) Both CD4+/CD8- and CD4-/CD8+ subsets of T lymphocytes decreased in TB- as well as MOTT- groups. However, the decrease in CD4+/CD8- subset was more manifest than that in CD4-/CD8+ subset. Among CD4+/CD8- subset the proportion of the Leu8+ subpopulation was slightly lower and among CD4-/CD8+ subset CD11b- subpopulation was slightly higher in both TB- and MOTT- groups than in healthy control group. 4) There was no significant difference in proportions of IL-2-receptor (p55 alpha chain) positive as well as HLA-DR positive T-lymphocytes between patient groups and healthy control group. 5) Both TB- and MOTT- groups were subdivided according to the extent of pulmonary lesion. Patients with the larger lesion showed remarkable decreases in the ratio of T lymphocytes to total peripheral leukocytes, the number of T lymphocytes, and the numbers of CD4+/CD8- and CD4-/CD8+ subsets, when compared with those with the smaller lesion. 6) Although the averages of absolute numbers of T lymphocytes, CD4+/CD8- and CD4-/CD8+ subsets were lower in patient groups than in the control group and the ratios of these to total lymphocyte counts and the ratio of CD4+ to CD8+ subsets were not significantly different between patient groups and control group, the distributions of each value of individual person were far broad in patient groups.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Flow cytometric analysis of peripheral T lymphocytes from patients with mycobacterial diseases]. 159 37

Cells of MPS and lymphatic system in lymph nodes from eighteen patients with culture proven tuberculous lymphadenitis were examined by histological and immunohistochemical technics. Ten patients suffered from symptomatic HIV-infection and eight patients were immunocompetent individuals without HIV serology. Characteristic granulomas with or without caseation were observed in the eight immunocompetent and the four HIV-infected patients with less marked lymphopenia of CD4 positive peripheral blood lymphocytes. In lymph nodes from the other HIV-infected patients with more severe depression of CD4 positive peripheral blood lymphocyte count no epitheloid cell formation was present. Instead of these cells foamy macrophages were found. The phenotype of macrophages underwent progressive changes parallel to decreasing numbers of CD4 positive peripheral blood lymphocytes. Foamy macrophages in mycobacterium avium-intracellulare infection may represent an end-stage phenotype. While many macrophages and lymphocytes expressed IL-2 receptors in cases with typical granulomas there was no such CD25 expression in cases without any epitheloid cell formation. Our results suggest that T-cell activation is necessary for epitheloid granuloma formation in human tuberculosis and preliminary in situ data support the assumption that in vivo the HIV-infection provokes an excess production of cytokines which in turn causes an exhaustion of the immune system and finally AIDS.
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PMID:[Immunohistochemical characterization of HIV-and non HIV-associated lymph node tuberculosis]. 172 23

Alveolar and lower respiratory tract immunity in addition to systemic immunity in 31 patients with pleural plaques found on chest X-rays were evaluated. All cases had occupational histories of asbestos exposure, but ferruginous bodies in BAL fluid were only detected in 21 of 31 cases. The percentage of cell components in BAL fluid was evaluated according to the number of ferruginous bodies found in the BAL fluid. As the number of ferruginous bodies increased, neutrophils and T lymphocytes decreased, but B lymphocytes increased. Furthermore, CD25-positive cells were remarkably increased in patients with high exposure to asbestos. In addition, CD25-positive cells in the peripheral blood and serum soluble IL-2 receptors were elevated in the patients with high exposure to asbestos.
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PMID:[Evaluation of immunity based on bronchoalveolar lavage fluid in patients with pleural plaque in the chest X-ray]. 175 18

Toxicity of environmental pollutants may be expressed as combined effects of a chemicals. Benzene, a proven hematotoxic agent, frequently occurs with toluene in cocontaminated groundwater. Groups of CD-1 male mice were exposed continuously for 4 weeks to benzene (166 mg/l), toluene (80 and 325 mg/l), and combinations of benzene (166 mg/l) + toluene (80 mg/l or 325 mg/l) in drinking water. Benzene-induced anemia was alleviated by simultaneous toluene treatment. Leukopenia and lymphopenia were observed in the case of benzene only and benzene + toluene (80 mg/l)-treated mice. The cytopenia, however, was less severe in the benzene + toluene (325 mg/l)-treated group. Immunotoxicity induced by benzene treatment alone was characterized by involution of thymic mass and suppressions of both B- and T-cell mitogeneses, mixed lymphocyte culture response to alloantigens, the tumor lytic ability of cytotoxic T-lymphocytes as determined by 51Cr-release assay, and antibody production response to T-dependent antigen (sheep red blood cells). IL-2 secretion by Con A-stimulated mouse T-cells was decreased in the benzene-treated group. Toluene (325 mg/l) completely inhibited these adverse effects when it was coadministered with benzene, while the low dose of toluene (80 mg/l) did not protect against benzene-induced depressions of immune functions. Toluene administered alone at levels up to 325 mg/l showed no obvious immunotoxic effects. Results of this study demonstrated that toluene, in sufficient amounts, has an antagonistic effect on benzene immunotoxicity.
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PMID:Subclinical effects of groundwater contaminants. III. Effects of repeated oral exposure to combinations of benzene and toluene on immunologic responses in mice. 214 47

Interleukin-2 (recombinant methionyl human interleukin-2 alanine 125; IL-2) was administered intralymphatically to 12 patients with advanced cancer in a phase I trial. Doses were administered once a week for 6 weeks in a dosage escalation schedule; patients were entered in four groups at successively higher starting dosages. Toxicity occurred in a profile similar to that seen with intravenous IL-2. The maximum tolerated dose with this route/schedule was 275,000 units/kg, a figure not higher than expected with intravenous administration. T1/2 alpha was prolonged to 54 min from the 13 min figure we obtained with IL-2 given intravenously. Granulocytosis and eosinophilia were seen, along with lymphocytosis following initial lymphopenia. Anti-IL-2 antibodies were seen in 42% of patients (compared to 16% with this agent given intravenously), suggesting increased immunogenicity of this route/schedule. No clinical response was achieved. Immunologic effects will be reported separately but are summarized.
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PMID:A pilot study of intralymphatic interleukin-2. II. Clinical and biological effects. 231 62

Subtoxic doses of endotoxin (salmonella abortus equi lipopolysaccharide, LPS) (5 micrograms/kg i.p.) or tumor necrosis factor alpha (TNF alpha) (15 micrograms/kg i.v.) induced fulminant hepatitis within 8 hr, when mice had been sensitized by a subtoxic dose of D-galactosamine (700 mg/kg i.p.). LPS-treatment led to the release of TNF into the circulation, independently of the presence of D-galactosamine. The TNF-dependent development of hepatitis was accompanied by a severe lymphopenia and neutrophilia as assessed by leukocyte differential count. The total leukocyte count was not significantly affected. Lymphopenia and neutrophilia were induced by LPS or TNF alpha alone; however, the differential count was not influenced by D-galactosamine. A quantity of 260 micrograms/kg phorbol myristate acetate (PMA) i.p. or 5 micrograms/kg platelet activating factor (PAF) i.v. or 3.3 mg/kg N-formyl-methionyl-leucyl-phenylalanine methylester (FMLP) i.v. or 167 mg/kg zymosan i.v. also caused lymphopenia and neutrophilia in mice. However, none of these agents induced the production of systemic TNF and therefore failed to induce hepatitis in D-galactosamine-sensitized mice. In LPS-insensitive C3H/HeJ mice administration of LPS produced neither differential count changes nor hepatitis while both events were observed when TNF alpha was given. This shows that TNF alpha alone gives rise to lymphopenia/neutrophilia as well as hepatitis independent of LPS. When the action of TNF alpha was blocked by anti TNF alpha antiserum pretreatment of LPS-sensitive mice, the animals were protected against LPS-induced hepatitis. However, lymphopenia and neutrophilia still occurred to a similar extent. The involvement of a putative additional mediator of LPS-induced leukocyte alterations was checked. The findings suggest that this mediator, if present, is different from IL-1, IL-2, eicosanoids or superoxide. We conclude from our findings that changes in leukocyte numbers and composition following D-galactosamine LPS or D-galactosamine/TNF alpha administration is an epiphenomenon rather than a causal event of leukocyte stimulation in the process of inducing a fulminant hepatitis in mice.
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PMID:Leukocyte alterations do not account for hepatitis induced by endotoxin or TNF alpha in galactosamine-sensitized mice. 240 85

HIV infection is known to induce a progressive T helper/inducer (CD4) lymphopenia and to impair the functional activities of residual cells. The present studies examined the relationship between the CD4 cell count and three functional assays: T cell colony formation in semisolid media, the capacity of PHA-stimulated cells to express IL-2 receptors, and their ability to synthesize and secrete IL-2. Cells from antibody-positive homosexuals with normal numbers of CD4 cells (greater than 700/microliters) showed defective reactivity in two assays, colony growth, and IL-2 receptor expression. These defects became progressively more pronounced in homosexuals with moderate (400-700 cells/microliters) and severe (less than 400/microliters) reductions in assays for IL-2 production by PHA-stimulated lymphocytes. Mixing experiments suggest that cells from HIV-infected men nonspecifically inhibit the colony growth of normal cells; this abnormality could be reversed by addition of exogenous IL-2. These data suggest that defective colony growth and reduced IL-2 expression are functional abnormalities directly resulting from HIV infection. Furthermore, these changes can precede the CD4 lymphopenia induced by this viral infection.
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PMID:Defective T cell colony formation and IL-2 receptor expression in HIV-infected homosexuals: relationship between functional abnormalities and CD4 cell numbers. 252 69

We previously demonstrated that IL-2 promotes the adhesion of NK cells to endothelial cells (EC) and that EC are readily lysed by lymphokine-activated killer (LAK) cells in vitro, suggesting that cell mediated endothelial injury may contribute to the capillary leak syndrome observed in patients treated with IL-2. In this investigation, we sought to determine the effects of EC activation on the in vitro susceptibility of EC to LAK cell-mediated cytolysis. Despite increased binding of CD16+ lymphocytes to TNF-activated EC monolayers, prior exposure of EC to any of several IL-2-inducible cytokines including TNF-alpha, IL-1 beta, and IFN-gamma not only failed to render the EC more vulnerable to cytolysis but increased their resistance to LAK cells in 111Indium release cytolysis assays. This decrement in susceptibility to cytolysis resulting from prior exposure to cytokines preceded any detectable increase in HLA class I or II Ag expression. In cold target competition experiments with LAK cell effectors and radiolabeled K562 target cells, TNF-primed EC were no more competitive than unstimulated EC, and in assays with unstimulated PBMC effectors, the addition of unlabeled TNF-activated EC actually increased the cytolysis of the radiolabeled tumor cells. The effects of various cytokines and lymphocyte preparations on EC permeability were also evaluated. In these experiments, saphenous vein EC were cultured on porous filter disks, exposed to cytokines or lymphocytes, and the diffusion of 125I-BSA through the filters was then measured. Exposure to IL-2, IFN-gamma, or TNF-alpha did not increase the diffusion of the BSA through the EC-coated filters, whereas LAK cells markedly increased their permeability. Consistent with the results of the cytolysis assays, pretreatment of the EC with TNF, IL-1, or IFN-gamma diminished the LAK cell-induced increase in BSA diffusion. These results suggest that although circulating IL-2-inducible cytokines such as TNF and IFN-gamma may activate EC in vivo and contribute to lymphocyte margination and lymphopenia, they may not be directly responsible for the IL-2-induced capillary leak syndrome and may actually protect EC from LAK cell-mediated injury.
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PMID:Activated endothelial cells resist lymphokine-activated killer cell-mediated injury. Possible role of induced cytokines in limiting capillary leak during IL-2 therapy. 252 94

The incidence of tuberculosis is very high in patients treated by hemodialysis particularly in the early stage of hemodialysis. The diagnosis of tuberculosis in dialysis patients was obscured as symptoms were nonspecific and extrapulmonary involvement was seen frequently. We investigated cell mediated immunity in dialysis patients in relation to the period of dialysis. The data indicate that dialysis patients show the following immunological impairments; 1) lymphopenia, 2) decreased B cell, 3) alteration of T cell subset, 4) decreased reaction of PPD skin test, 5) decreased T cell activity, 6) decreased IL-2 production, 7) decreased PHA induced lymphocyte blastogenesis, 8) decreased NK cell. Decreased immunologic host defence mentioned above may contribute to the high incidence of tuberculosis in the early stage as well as in the maintenance phase of dialysis.
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PMID:[Tuberculosis in patients undergoing hemodialysis]. 281 Oct 1


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