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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied a number of parameters, which may all depend upon cytoskeletal function, comparing lymphocytes and granulocytes (PMN) from young and old healthy donors. F-actin content was measured by NBD-phallacidin staining, followed by flow cytometry and was expressed as mean channel fluorescence (MCF). There were no differences in the basal F-actin content of PMN obtained from young (under 35 years old) and old donors (above 65 years). In contrast, the basal F-actin content was higher in lymphocytes obtained from the old donors (MCF, 56.8 +/- 2.9 vs 48.1 +/- 2.6 in the young; mean +/- SEM, n = 20, p less than .03). Stimulus-induced actin polymerization was slightly lower in the older age-group both in PMN and lymphocytes, but a significant difference was found only in PMN stimulated with the chemotactic peptide, N-formyl-methionyl-leucyl-phenylalanine (MCF 97.9 +/- 4.7 vs 88.6 +/- 3.4; young vs old, mean +/- SEM, n = 20, p less than .05). Interleukin-2 receptor expression was measured by staining with FITC-conjugated anti-CD25 antibodies and flow cytometry, following stimulation with phytohemagglutinin (PHA) or pokeweed mitogen (PWM). Perturbation of the cytoskeletal system with pentoxifylline, which has been shown to decrease F-actin content and inhibit the expression of several cell surface receptors, had similar effects on leukocytes from young and old donors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Age-related alterations in actin cytoskeleton and receptor expression in human leukocytes. 153 58

Soluble CD25 antigen was measured in 28 patients with Graves' disease and 20 patients with thyroid autonomy in order to address the question of whether this parameter could be used in the differential diagnosis of thyrotoxicosis. Soluble CD25 was significantly elevated in active Graves' disease (2430 +/- 442 U/ml, mean +/- SEM) compared to patients with thyroid autonomy (1295 +/- 225 U/ml, mean +/- SEM). However, compared to normal controls (mean 605 +/- 49 U/ml), both groups of patients had significantly elevated CD25 plasma levels. Investigations in thyroidectomized thyroid cancer patients on and off T4 suppressive therapy showed no influence of T4 on the CD25 level. Soluble CD25 concentrations did not differ in thyroid cancer patients compared to normal controls. We conclude that soluble CD25 may indicate a stimulation of the immune system with high sensitivity; however, due to the low specificity of elevated CD25 levels, its usefulness for differential diagnosis of thyrotoxicosis is limited.
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PMID:Is soluble CD25 antigen (interleukin-2 receptor) a useful parameter for differential diagnosis of thyrotoxicosis? 160 Mar 37

Age and elevated blood pressure are associated with blunted beta-adrenoceptor-mediated cardiovascular effects. To investigate a possible relationship between beta-adrenoceptor cardiovascular function and receptor density, beta-adrenoceptor binding capacity in mononuclear leucocytes and cardiac isoproterenol sensitivity were compared in 12 essential hypertensive and 17 normotensive subjects of comparable age. The bolus dose of isoproterenol which increased heart rate by 25 beats/min (CD25) as well as plasma norepinephrine, epinephrine, and renin activity were measured. In a radioreceptor assay using [3H]dihydroalprenolol, the antagonist binding capacity (Bmax) and the affinity constant (KD) of mononuclear leucocytes were determined. Bmax in patients was higher than in normotensive subjects (66.8 +/- 4.1 versus 48.0 +/- 3.8 SEM fmol/mg, p less than 0.05), and KD was identical in both groups. In hypertensive patients, Bmax correlated positively with age (r = 0.639, p less than 0.05) and CD25 (r = 0.593, p less than 0.05) and negatively with plasma renin activity (r = 0.679, p less than 0.05), while in normotensive subjects, Bmax correlated with CD25 only (r = 0.615, p less than 0.05). Thus, in patients with essential hypertension, a decrease in cardiac isoproterenol sensitivity and plasma renin activity is associated with an age-related increase in antagonist binding capacity. This suggests a defect in the membrane coupling of the beta-adrenoceptor effector system distal to the receptor recognition site in patients with essential hypertension.
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PMID:Increased beta-adrenoceptor binding capacity is associated with blunted beta-adrenoceptor-mediated cardiovascular responses in essential hypertension. 241 82

We compared the effects of single doses of 50 mg atenolol (cardioselective), 40 mg propranolol (nonselective), and placebo on both exercise- and isoproterenol-induced tachycardia in two experiments involving nine normal subjects. Maximal exercise heart rate was reduced from 187 +/- 4(SEM) after placebo to 146 +/- 7 bpm after atenolol and 138 +/- 6 bpm after propranolol, but there were no differences between the drugs. The effects on isoproterenol tachycardia were determined before and after atropine (0.04 mg/kg IV). Isoproterenol sensitivity was determined as the intravenous dose that increased heart rate by 25 bpm (CD25) and this was increased from 1.8 +/- 0.3 micrograms after placebo to 38.9 +/- 8.3 micrograms after propranolol and 8.3 +/- 1.7 micrograms after atenolol. The difference in the effects of the two was significant. After atropine the CD25 was unchanged after placebo (2.3 +/- 0.3 micrograms) and atenolol (7.7 +/- 1.3 micrograms); it was reduced after propranolol (24.8 +/- 5.0 micrograms), but remained different from atenolol. This change with propranolol sensitivity was calculated as the apparent Ka, this was unchanged by atropine (11.7 +/- 2.1 and 10.1 +/- 2.5 ml/ng). These data are consistent with the hypothesis that exercise-induced tachycardia results largely from beta 1-receptor activation that is blocked by both cardioselective and nonselective drugs, whereas isoproterenol activates both beta 1- and beta 2-receptors so that after cardioselective blockade there remains a beta 2-component that can be blocked with a nonselective drug. While there appear to be beta 2-receptors in the human heart, their physiologic or pathologic roles remain to be defined.
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PMID:Evidence for cardiac beta 2-adrenoceptors in man. 629 41

The immune dysfunction in human immunodeficiency virus (HIV) infection is complex and cannot be explained solely on the basis of numerical depletion of T lymphocytes. Inappropriate, uncontrolled activation of the immune system may be involved. In a test of this hypothesis, five HIV-infected children were prospectively treated with prednisone and selected immunologic and virologic indices were analyzed. Subjects had marked T lymphopenia (CD4+ T lymphocytes < 500 cells/ml) and antigenemia (serum p24 antigen > 30 pg/ml) and were free of opportunistic infections. There was a significant drop in serum p24 antigen concentrations from baseline (60.2 +/- 10.1% SEM; P < 0.005) 4 weeks after initiation of prednisone, which returned to baseline concentrations as the prednisone was tapered. Concomitant with this decrease, there was decreased expression of cell surface activation markers (HLA-DR, CD25 (interleukin 2 receptor) and CD26 (Ta-1)) in peripheral T lymphocytes. There was no significant change in either T lymphocyte subset numbers or mitogen and antigen-specific lymphoproliferation. A regulatory dysfunction of the immune system, allowing inappropriate activation of T lymphocytes, may be involved in the pathogenesis of HIV disease, and further studies involving selective immunosuppression in HIV disease are warranted.
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PMID:Immunologic and virologic effects of glucocorticoids on human immunodeficiency virus infection in children: a preliminary study. 790 39

T lymphocyte activation after leukocyte membrane interaction may play a role in immune dysfunction associated with hemodialysis (HD). Studies of T-lymphocyte activation markers in HD have yielded conflicting results, perhaps due to the use of a limited number of markers and different measurement techniques. We studied the lymphocyte activation markers CD25 (interleukin-2 receptor), CD38, CDw49b (VLA-2), CD71 (transferrin receptor), and HLA-DR, as well as the surface antigens CD3, CD4, CD7, and CD8 by two-color flow cytometry in 23 chronic HD patients before and after a single dialysis session; we also studied 30 normal controls. There was no increase in the percentage of activated T cells in the controls and in the patients pre- and post-HD. Conversely, the percentage of CD3+/CD71+ (transferrin receptor) cells was significantly decreased in the patients pre-HD compared with the controls (3.6% +/- 0.5% [mean +/- SEM] v 5.9% +/- 0.5%; P < 0.005). A single dialysis session did not alter the percentage of activated subsets, but led to significant depletion in the number (x 10(9)/L) of cells that were CD3+ (1.10 +/- 0.10 v 0.97 +/- 0.09; P < 0.05), CD7+ (1.0 +/- 0.09 v 0.85 +/- 0.08; P < 0.0001), and CD8+ (0.50 +/- 0.06 v 0.37 +/- 0.04; P < 0.001), but not CD4+ cells (0.73 +/- 0.08 v 0.69 +/- 0.07; P = NS). These data indicate that the chronic HD patients at baseline "predialysis" do not appear to have an increased percentage of circulating activated T lymphocyte subsets and that the CD3+/CD71+ subset is in fact decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Activated and regulatory T lymphocyte populations in chronic hemodialysis patients. 791 75

TGF-beta 1 is known to modulate lymphocyte activation affecting cell proliferation and the production of cytokines and Igs. Little is known about the characteristics of T cells grown in the presence of TGF-beta 1. We have stimulated human T cells with PHA in the presence of TGF-beta 1 under serum-free conditions for 7 days and characterized the resulting cell population. TGF-beta 1 (0.0032 to 10 ng/ml) affected neither [3H]thymidine incorporation (day 4) nor cell yield (day 7) in these cultures. However, cells activated in the presence of TGF-beta 1 proliferated vigorously in secondary cultures and produced highly elevated amounts of IL-2 (12 +/- 3-fold enhancement of IL-2 production in response to CD2 plus CD28 stimulation compared with control cells, mean +/- SEM; n = 10). The enhancing effects of TGF-beta 1 were demonstrable over a wide range of concentrations (0.4 to 10 ng/ml). The increased IL-2 protein production was paralleled by a dramatic up-regulation of IL-2 mRNA. In addition, cells precultured with TGF-beta 1 responded with enhanced cluster formation in the secondary cultures. With regard to their phenotype, we observed an increased expression of the alpha E beta 7-integrin human mucosal lymphocyte-1 and of the CD2-restricted epitope CD2R, whereas the expression of CD11a was slightly decreased. In contrast, TGF-beta 1 did not influence the constitutive or activation-induced expression of CD4, CD8, CD45RA, CD45RO, CD25, CD71, CD54, CD58, CD59, and B7. We conclude that TGF-beta 1 supports the generation of human effector cells with a strongly enhanced capacity to respond to subsequent restimulation.
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PMID:TGF-beta 1 is a potent inducer of human effector T cells. 796 15

Alveolar macrophages (AMs) harvested from 32 HIV-infected patients with respiratory problems (opportunistic pulmonary infections, n = 12; other lung disease, n = 20) and 13 healthy controls were stained with a panel of 15 monoclonal antibodies directed against surface antigens implicated in cell function. Antigen expression was quantified by flow cytometry and expressed as relative linear median fluorescence intensity (RLMFI). On AMs of patients, as compared with controls, there was a significant enhancement of HLA DP (12.1 +/- 1.5 vs 6.5 +/- 0.9, p = 0.01, M +/- SEM, RLMFI units), CD11b (3.4 +/- 0.5 vs 1.7 +/- 0.4, p = 0.014), CD11c (8.9 +/- 1.0 vs 4.8 +/- 0.8, p = 0.0046), CD14 (2.1 +/- 0.3 vs 1.0 +/- 0.2, p = 0.0009), and CD33 (1.7 +/- 0.1 vs 1.0 +/- 0.2, p = 0.0093). No significant differences could be established for HLA-DR (36.9 +/- 5.8 vs 30.9 +/- 7.5, NS), HLA-DQ (3.4 +/- 0.3 vs 3.1 +/- 0.6, NS), CD54 (1.9 +/- 0.3 vs 1.2 +/- 0.1, NS), CD13 (2.5 +/- 0.6 vs 1.5 +/- 0.3, NS), CD36 (1.4 +/- 0.2 vs 0.9 +/- 0.3, NS), CD71 (10.3 +/- 1.9 vs 8.9 +/- 1.8, NS), CD25 (0.8 +/- 0.0 vs 0.9 +/- 0.1, NS), 27E10 (1.1 +/- 0.1 vs 0.8 +/- 0.3, NS), RM3/1 (1.9 +/- 0.4 vs 1.5 +/- 0.4, NS), and CD4 (1.5 +/- 0.3 vs 1.0 +/- 0.0, NS). The expression of CD14 and CD11b, but not of HLA class II antigens and CD71, was increased in the smaller cell population compared with the larger, thus suggesting monocyte recruitment. The increased expression of HLA-DP, CD11c, CD14, and CD33 on the patients' AMs was independent of smoking habits. The degree of immunodeficiency as indicated by the absolute peripheral CD4 count, the character of HIV-related pulmonary disease, and the prophylactic use of pentamidine or zidovudine did not significantly modify the antigen expression pattern. It is concluded that HIV infection may lead, most probably indirectly, to enhanced expression of surface antigens by local upregulation and/or recruitment of monocytes from the peripheral circulation. The functional significance of enhanced marker expression requires further clarification.
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PMID:Expression of surface markers on alveolar macrophages from symptomatic patients with HIV infection as detected by flow cytometry. 818 14

In vitro effects of human recombinant IL-6 (1-1000 U/ml) on highly enriched human NK CD3-CD56+ cells (94% +/- 2; mean +/- SEM; n = 8), obtained from PBL were studied. IL-6 induced low levels of NK cell proliferation (7- to 30-fold during 6-day incubation), which was IL-2-independent, because IL-6 did not induce detectable IL-2 production by NK cells. Two-color flow cytometry analysis demonstrated that incubation of NK cells with IL-6 at the optimal concentration of 250 U/ml for 6 days significantly increased the proportion of NK cells expressing the following activation Ag: CD25 (26% +/- 17, mean +/- SEM vs 4% +/- 1 in control, n = 5), CD54 (44% +/- 17 vs 9% +/- 3), HLA-DR (29% +/- 13 vs 12% +/- 4), CD69 (45% +/- 7 vs 12% +/- 3), and CD71 (34% +/- 17 vs 6% +/- 2). The mean fluorescence intensity of these activation Ag was increased as well. IL-6 induced expression of CD49b (alpha-chain of VLA-2, 20% +/- 11 vs 2% +/- 1) and CD49c (alpha-chain of VLA-3, 43% +/- 17 vs 5% +/- 3), which are not expressed on resting NK cells. IL-6 also enhanced the fluorescence intensity of beta 1 integrins, CD49d, CD49e, and CD49f, expressed on NK cells. IL-6-stimulated NK cells showed significantly increased integrin-mediated adhesion to fibronectin- or laminin-coated plates (26 +/- 3 mean % cells adhering +/- SEM vs 15 +/- 4 in control for FN and 19 +/- 1 vs 11 +/- 1 for LM, p < 0.05 for both) as determined in a 3 h binding assay. As assessed by inhibition of adhesion using mAb to the VLA-2, -3, -4, -5, and -6, NK cell adhesion to fibronectin was mediated by VLA-4 and 5, and their adhesion to laminin by VLA-3 and -6. NK cells incubated in the presence of IL-6 were found to produce a factor cytostatic to WEHI-164 clone 13 target cells. This effect was partly, although significantly, blocked by neutralizing antibodies to TNF-alpha or TNF-beta. Our data demonstrate that IL-6 can directly activate human NK cells, but is a less potent NK cell activator, for all activation and functional parameters studied, than IL-2.
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PMID:Response of human NK cells to IL-6 alterations of the cell surface phenotype, adhesion to fibronectin and laminin, and tumor necrosis factor-alpha/beta secretion. 849 90

Sputum examination is a useful noninvasive method to study airway inflammation. We investigated the reproducibility and validity of the measurements of lymphocyte subsets in the sputum of 11 stable patients with asthma and 10 nonasthmatic smokers. Sputum was dispersed with 0.1% dithiothreitol. A differential cell count was made with Wright's stain. Aliquots were stained with antibodies to CD19 (B cells), CD3 (T cells), CD4 (helper), CD8 (suppressor), and the activation marker CD25 (IL2 receptor) on T-cell subsets and were assayed by flow cytometry. Sputum from patients with asthma compared with nonasthmatic subjects had more eosinophils (mean +/- SEM, 32.5 +/- 8.5 versus 1.3 +/- 0.5%, p < 0.01) and a higher proportion of lymphocytes that were B cells (16.2 +/- 3.2 versus 4.0 +/- 1.0%, p < 0.01), and these correlated closely with the eosinophils (r = 0.8, p < 0.01). Patients with asthma also had more activated T-helper cells (39.3 +/- 4.6 versus 9.0 +/- 9.0%, p = 0.05), but the comparison was limited to two smokers because of macrophage autofluorescence. The repeatability of measurements of helper T-cells (R = 0.94), suppressor T cells (R = 0.88), and activated helper T cells (R = 0.77) was good; repeatability of measurements of T and B cells could not be examined because these were reciprocals of each other. Asthmatic sputum has different lymphocyte profiles than sputum from nonasthmatic smoking control subjects. The results demonstrate a potential importance of antibody-producing lymphocytes in the airway and their relation to sputum eosinophilia in asthma.
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PMID:Elevated B cells in sputum of asthmatics. Close correlation with eosinophils. 856 94


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