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)

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

This study examined the relationship between exercise-induced changes in the concentration of circulating immunocompetent cells and their surface expression of adhesion molecules: L-selectin (CD62L) and three beta 2-integrins [LFA-1(CD11a/CD18), Mac-1 (CD11b/CD18), and p150/95(CD11c/CD18)]. Eight young male volunteers exercised on a cycle ergometer for 60 min at 60% maximal oxygen uptake. Peripheral blood samples, collected every 30 min throughout exercise and during the 2-h recovery period, were used for flow-cytometric analysis. The experimental results were compared with control data obtained ever 60 min at corresponding times of the nonexercise day. The exercise regimen induced a granulocytosis and a lymphocytosis, mainly due to an elevation of CD8+ and CD16+ cells. During recovery, a further granulocytosis occurred but accompanied by a lymphopenia. The increased CD8+ cell-count during exercise was characterized by a selective mobilization of the CD62L- and CD11ahigh cells, i.e. primed CD8+ cells. A postexercise suppression of CD4+ cell-count was derived only from CD62L+ cells. The CD11b+ and CD11c+ lymphocytes also increased during exercise, largely attributable to an increase in CD16+ cells which co-expressed CD11b and CD11c molecules. The CD62L surface density of granulocytes increased significantly during recovery. This resulted from a selective influx of CD62Lhigh granulocytes into the circulation. There were no significant changes in per-cell density of the three beta 2-integrins on granulocytes and lymphocytes throughout the experimental period. These results suggest that the cell-surface expression of CD62L (and CD11a) molecules is associated with the differential mobilization of CD8+ cells during exercise, the postexercise suppression of CD4+ cell-counts and the granulocytosis following exercise.
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PMID:Exercise-induced changes in the expression of surface adhesion molecules on circulating granulocytes and lymphocytes subpopulations. 758 96

In 13 middle-aged, moderately trained men (40-60 yr) we investigated the influence of anaerobic training on immunological parameters measured at rest. The 4 week anaerobic training program (two 30-min sessions weight lifting and one interval training per week; lactate levels 4-6 mM and 8-10 mM, respectively), caused a significant increase of the mean arm muscle force by 7% (handgrip test, p < 0.05). Evaluation of lymphocyte subsets was performed by means of three-colour immunofluorescence analysis (FACS). After 4 weeks of training we found a significant reduction of the CD4+ T-cell counts by 15% (p < 0.05) paralleled by a fall of naive cells (CD3+/CD4+/CD45RA+) by 16%, which, however, was statistically not significant. While percentages of CD3+ lymphocytes decreased significantly by 6% (p < 0.001), absolute numbers of CD3+ T-lymphocytes were not detectably affected and also the relative ratio of CD8+ T-cell subsets, i.e. the ratio of suppressor vs cytotoxic T-cells (CD3+/CD8+/CD11b+, CD3+/CD8+/CD11b- respectively) remained unchanged. Likewise the serum concentrations of the soluble CD8 and CD4 antigen (sCD8/sCD4) as determined by sandwich enzyme immunoassays were found to be unaffected. We conclude that 40-60 years old healthy human subjects performing anaerobic training experience on average a significant decrease of circulating CD4+ T-lymphocytes, while other parameters including the activation parameters sCD8 and sCD4 remained unchanged.
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PMID:Lymphocyte subpopulations and concentrations of soluble CD8 and CD4 antigen after anaerobic training. 775 Oct 74

Endotoxin challenge causes metabolic dysfunction mediated by TNF, and sequestration of leukocytes. NPC 15669, N-carboxy-L-leucine, N-[2,7-dimethylfluoren-9-yl)methyl] ester, inhibits leukocyte recruitment into inflammatory lesions in animals, and inhibits endotoxin-induced neutropenia and lymphopenia in mice. This study was carried out to determine whether the ability of NPC 15669 to inhibit leukocyte sequestration is sufficient to promote survival after endotoxin challenge. To inhibit leukocyte sequestration directly, mice were treated with anti-CD11a (LFA-1) or anti-CD11b (Mac-1) before endotoxin challenge. Anti-CD11b partly inhibited neutropenia and lymphopenia in response to challenge with LPS, but anti--CD11a had little effect on leukopenia. At doses of 100 and 1000 micrograms/kg, anti-CD11b increased survival to endotoxin challenge from 0 to 20 and 40%, respectively, whereas anti-CD11a was without effect. These observations, coupled with the finding that NPC 15669 does not inhibit endotoxin-induced TNF release suggest that inhibition of leukocyte sequestration can increase survival after endotoxin challenge, and that NPC 15669 or antibodies to Mac-1 may represent effective therapies for gram-negative sepsis and shock.
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PMID:Mice treated with a leumedin or antibody to Mac-1 to inhibit leukocyte sequestration survive endotoxin challenge. 846 78

Murine CD3/T cell receptor (TCR) monoclonal antibodies (mAbs) induce immediate peripheral lymphocytopenias of different degree and duration. Lymphocytopenia is of short duration after the administration of immunoglobulin A CD3 mAb, but it persists much longer after the administration of immunoglobulin G2a CD3 mAb. Peripheral lymphocytopenia after the administration of WT31, a murine immunoglobulin G1 TCR mAb, appears to be dependent on the polymorphism of Fc(gamma)RIIa. In high responders, lymphocytopenia is comparable to that observed after immunoglobulin G2a CD3 mAb; in low responders, no lymphocytopenia occurs. In vitro, both immunoglobulin A and immunoglobulin G2a CD3 mAbs induce immediate activation of CD11a/CD18, with concomitant up-regulation of CD11b/CD18 on T cells, each of which is shown to be involved in the concurrent adhesion of T cells to endothelium. WT31 induces an immediate activation of CD11a/CD18 as well as T cell adhesion to endothelium in Fc(gamma)RIIa high responders only, interestingly without changes in the level of expression of CD11b/CD18. We conclude that the immediate occurrence of peripheral lymphocytopenia after the administration of CD3/TCR mAb is mediated by changes in the level of expression or avidity (or both) of adhesion molecules on T cells, whereas the persistence of this lymphocytopenia depends on the isotype of the CD3/TCR mAb and on the presence of suitable Fc receptors.
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PMID:Different CD3/T cell receptor monoclonal antibodies have distinct capacities to induce adhesion of T lymphocytes to endothelium. 924 71

We investigated the distribution of B and T cells in the peripheral blood of haematologically inconspicuous (non-persistent lymphocytotic, PL-) cattle infected with the bovine leukaemia virus (BLV). Flow cytometric data were obtained from six PL- cattle and compared with six age-matched animals with persistent lymphocytosis (PL+) and five non-infected healthy controls (BLV-). In the PL- group, the percentage and number of surface immunoglobulin-positive (sIg+) B cells were significantly reduced. Whereas in BLV-cattle, about 40% of the peripheral blood lymphocytes (PBL) were sIg + and 24% were sIgM + B cells. In the PL- group, less than 20% of the PBL were sIg+ and sIgM+ B cells. Only 5% of the PBL co-expressed sIgM+ and CD5+ versus 16% in BLV-. This decrease was persistent over 3 years and predominantly affected: (i) B cells that did not express sIgM; (ii) sIgM + B cells co-expressing CD5 and CD11b; and (iii) equally both lambda- and K-type light chain B-cell subpopulations. In contrast, the number of all circulating lymphocytes, CD5- and CD11b- sIgM+ B cells and CD2+ T cells did not differ. In PL+ animals, about 75% of the PBL were sIgM+ CD5+ B cells. These cells were of polyclonal origin, as light chains of the lambda- and K-type were expressed in a ratio of 4:1 (57.7% of PBL lambda+, 14% kappa+) as in BLV- animals (33.6% of PBL lambda+, 8.7% kappa+). In PL+ cattle the absolute number of B-cells and, therefore, their relative percentage is significantly increased. For this reason, even in case of absolutely increased T-cell numbers, the relative percentage of T-cells could be lower than in normal controls. The cause for the observed B cell decrease in PL- cattle is unknown, but it can be assumed that cytotoxic T cells are involved in this B-cell lymphopenia.
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PMID:Cattle infected with bovine leukaemia virus may not only develop persistent B-cell lymphocytosis but also persistent B-cell lymphopenia. 1224 Oct 26

Social stress of group-housed male mice induced a state of functional glucocorticoid (GC) resistance in splenocytes. The following studies examined the effects of paired-fighting (PF) stress on immune cell distribution and function in spleens of male mice. Following six daily PF stress sessions, splenic monocytes and neutrophils increased and lymphocytes decreased. PF also altered the distribution of CD62L and CD11b positive monocytes. Additionally, PF augmented proliferation and lowered the sensitivity of LPS-stimulated splenocytes to the antiproliferative effects of corticosterone, suggesting that PF induced a state of GC resistance in splenocytes. Together, these findings indicate that social stress altered phenotype and function of splenic immune cells. These findings may have implications for the healing of bite wounds that are often associated with social stress in rodents.
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PMID:Social stress alters splenocyte phenotype and function. 1241 35

Suboptimal nutriture causes leukopenia, but whether this is related to a modification in hematopoiesis is unknown. A 34-d period of zinc deficiency was used to obtain moderate and severely zinc-deficient (ZD) young adult mice whose bone marrow was evaluated for alterations in hematopoiesis, myelopoiesis and lymphopoiesis by flow cytometry. Expressions of CD31 (PECAM-1) and Ly-6C were used to identify changes in marrow population composition. Identity of marrow cells was confirmed with TER119, CD45R, Ly-6G and CD11b. Cells of the erythroid lineage declined as much as 60% depending on the degree of zinc deficiency, providing new insight into the early observations of clinicians that anemia accompanied ZD in humans. The lymphoid compartment also declined 50-70% with preferential losses among pre-B cells, an underlying cause of the lymphopenia that is a part of ZD, in which loss of pre-B cells was identified by CD43,CD45R, and immunoglobulin M. Conversely, cells of the myeloid lineage increased substantially in the marrow, both in proportion and absolute numbers in all ZD mice. Granulocytic cells increased 40-60%, whereas monocytic cells nearly doubled in ZD mice. These data suggest that there are important adaptations in hematopoietic functions as zinc becomes limiting. In the immune system, the precursors of phagocytic cells, which provide innate immunity, are protected, whereas precursors of lymphocytes, which provide adaptive immunity, are down-regulated. These findings illuminate the unique response of the marrow to a nutritional stress.
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PMID:Zinc deficiency in mice alters myelopoiesis and hematopoiesis. 1242 43

Extracorporeal support during cardiac surgery initiates an inflammatory response, causing damage to cardiac, pulmonary and renal tissue [Post Pump Syndrome (PPS)]. This is accompanied by a neutrophil leucocytosis and lymphopenia, but less is known about the role of monocytes and markers of monocyte activity. We studied 19 patients undergoing cardiac surgery, obtaining blood samples from the aortic root (AR) and from the coronary sinus ( < s) before the cardiopulmonary bypass (CPB), 1 min after release of the aortic crossclamp and 10 min after weaning from CPB (periods 1, 2 and 3). Leucocyte count, monocyte count and HLA-DR, CD15, CD11b and CD62L activation markers were measured. In samples obtained from the coronary sinus (CS), HLA-DR, expressed as a percentage of the monocyte count, decreased between periods 1, 2 and 3 by 78%, 66% and 43%, respectively. A similar change was observed in samples from the AR. Conversely, CD62L increased in the CS samples (55%, 68% and 73%), but revealed a lesser increase in the AR samples (51%, 68% and 63%). The other markers showed little change throughout the procedure. Reduced immunological competence could result from the decrease in HLA-DR counts. Increases in CD62L sensitizes monocytes to the tethering effects of endothelial integrins and might contribute to the atherosclerotic process.
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PMID:Monocyte activation markers during cardiopulmonary bypass. 1286 85

The popularly exploited murine neonatal thymectomy experimental autoimmune gastritis (nTx:EAG) model requires the animal to be in a state of lymphopenia. Here we report on a novel murine immunization (without adjuvant) model that can establish a lasting gastritis. We demonstrate that the immunization model (imm:EAG) results in a bona fide autoimmune disease and define the resulting pathology and serology observed and compare it with that reported for human autoimmune gastritis. Immune cells present in the stomachs of imm:EAG gastritic mice include CD8 T cells, CD11b and Gr1 (granulocytes/monocytes) and B cells. We detected circulating antibodies of immunoglobulin G1 (IgG1) subclass, with some IgG(2a) and IgG(2b) reactive to stomach membranes and the parietal cell proton pump. The class and subclass of autoreactive antibodies resulting from imm:EAG suggest a T helper 1 (Th1)/Th2 immune response. We establish that both self-reactive T and B cells from BALB/cCrSlc imm:EAG gastritic mice have the potential to induce a gastritis in BALB/c syngeneic nu/nu recipients. We conclude that this model is likely to be superior to the currently popularly exploited nTx:EAG and provide insight into and an understanding of the mechanisms of and remedies for autoimmunity in an intact immune system.
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PMID:Gastritis in neonatal BALB/cCrSlc mice induced by immunization without adjuvant can be transferred to syngeneic nu/nu recipients. 1639 1


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