UNIPROT:P08758 - FACTA Search

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Query: UNIPROT:P08758 (annexin V)
9,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Measles is associated with immunosuppression and increased susceptibility to secondary infections and is a particular problem in developing countries. Lymphocyte changes accompanying immune activation and regulation of the immune response may contribute to immunosuppression. To evaluate lymphocyte changes during measles, children (n = 274) hospitalized with measles in Lusaka, Zambia, were evaluated at entry, discharge, and 1-month follow-up and compared to healthy Zambian children (n = 98). Lymphopenia was present on hospital admission and reflected decreased CD4 and CD8 T cells but resolved quickly. Lymphopenia was most marked in girls, in those with temperatures of >38.5 degrees C, and in malnourished children. CD4/CD8 ratios were decreased at all time points and were lower in boys than in girls at discharge and follow-up. Spontaneous death occurred in cultured lymphocytes, and the proportions of freshly isolated cells undergoing apoptosis, based on annexin V and propidium iodide staining, were increased. Surface Fas was increased on both CD4 and CD8 T cells compared to controls, and expression was greater on CD4 T cells and was inversely correlated with lymphocyte viability in culture at study entry. Mitogen stimulation of lymphocytes improved viability, but inhibitors of Fas, tumor necrosis factor (TNF)-related apoptosis-inducing ligand, and TNF did not. Plasma levels of beta(2) microglobulin and soluble Fas, Fas ligand, CD8, CD4, and TNF receptor were increased, and soluble CD8 was higher in boys than in girls. The multiple effects of measles on lymphocytes from Zambian children include decreased numbers in circulation, increased activation, and increased susceptibility to cell death, with substantive differences in the magnitude of these changes between boys and girls.
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PMID:Functional and phenotypic changes in circulating lymphocytes from hospitalized zambian children with measles. 1220 49

The activation of circulating polymorphonuclear neutrophils (PMN) from patients with active tuberculosis (TB-PMN) may be associated with induction of apoptosis. Spontaneous or Mycobacterium tuberculosis (MTB)-induced apoptosis of PMN were evaluated by microscopy, DNA content, and their binding to Annexin V at 0, 3, and 18 h. In addition, the expression of CD11b and of CD16 were evaluated as parameters of activation and apoptosis, respectively. Recently isolated TB-PMN showed a higher CD11b expression than normal PMN (N-PMN), but there were no features of apoptosis, even though an enhancement of Fas expression was observed. Spontaneous apoptosis was accelerated in TB-PMN at 3 h, but no differences were observed in TB- and N-PMN at 18 h of culture. When stimulated with MTB, both TB- and N-PMN steadily increased CD11b expression along the culture period. MTB induced apoptosis of N-PMN at 3 h with loss of CD16 expression. By contrast, MTB delayed the apoptotic rate of TB-PMN, preserving the CD16 receptor at 3 h, whereas it accelerated apoptosis at 18 h, increasing at the same time the expression of CD11b. Taken together, these data suggest that the acceleration of apoptosis observed in TB-PMN could be associated with the MTB-induced activation.
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PMID:Mycobacterium tuberculosis-induced activation accelerates apoptosis in peripheral blood neutrophils from patients with active tuberculosis. 1239 18

The role of lymphocyte apoptosis in septic shock remains a controversial issue. Using Annexin V and flow cytometry analysis on freshly isolated cells, we evaluated circulating lymphocyte apoptosis in 23 septic shock, 25 sepsis without shock, 7 nonseptic critically ill, and 25 control patients. In patients with sepsis, we compared day 1 lymphocyte apoptosis (i.e., within 3 days of the onset of infection) with that observed 5-7 days after (day 6) according to shock state, mortality, and seventy factors. At day 1, patients in septic shock exhibited higher lymphocyte apoptosis than that present in controls (16.5% +/- 3.5% vs. 3% +/- 0.5%, respectively, P = 0.0001). At day 6, patients with sepsis without shock restored undamaged CD4+ T and CD8+ T lymphocyte counts, whereas patients in septic shock increased only CD4+ T cells. Similarly, survivors restored undamaged lymphocyte count at day 6 (+70%, P < 0.001), whereas nonsurvivors did not. Day 6 undamaged lymphocyte count negatively correlated with day 1 SAPS II, day 6 LOD score, mechanical ventilation, and ICU stay duration. We observed no apoptotic effect of septic shock plasma or septic shock circulating mononuclear cells on target lymphoid cell lines. We found no alteration in any death receptors Fas, TRAIL-R1, TRAIL-R2, or in their ligands on circulating blood cells. Catecholamines and interleukin 10 levels significantly increased in patients with septic shock, but did not correlate with apoptosis levels. We conclude that lymphocyte apoptosis is rapidly increased in blood of patients in septic shock and that lymphocyte apoptosis leads to a profound and persistent lymphopenia associated with poor outcome. These results suggest that lymphocyte apoptosis is one of the main components of human septic shock immune dysfunction and could be related more to microcirculatory disturbance than to circulating factors.
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PMID:Early circulating lymphocyte apoptosis in human septic shock is associated with poor outcome. 1246 54

Apoptosis plays a major role in tissue transplantation because intact T-cell-apoptosis pathways are required for the induction of tolerance to allografts. Moreover, immunosuppressive agents commonly used in clinical transplantation medicine promote lymphocyte apoptosis inhibiting the expression and production of cytokines involved in lymphocyte survival. The aim of our study was to evaluate peripheral blood mononuclear cells (PBMC) spontaneous apoptosis in patients undergoing chronic immunosuppressive treatment after cardiac transplantation. PBMC obtained from patients (n = 31) and controls matched for age and sex (n = 25) were cultured for 72 h and apoptosis was evaluated by quantification of fragmented DNA, staining with Hoechst 33258 dye and annexin V binding. We also investigated Fas expression and FasL mRNA expression as well as the ability of an IgM anti-Fas antibody to induce apoptosis. Finally, we evaluated IL2 production induced by PHA and the ability of IL2 to prevent apoptosis. In patients, PBMC underwent enhanced spontaneous apoptosis in comparison with controls. However, we could not find any difference between patients and normals as regards the expression of Fas and of FasL mRNA, even if the cross-linking of the Fas molecule induced apoptosis in PBMC from patients, whereas it failed to induce cell death in normals. We also found that IL2 production was significantly decreased in patients and that the addition of IL2 to the culture medium reduced PBMC spontaneous apoptosis. Our findings suggest that in cardiac transplanted patients PBMC undergo enhanced spontaneous apoptosis, which may contribute to prevent allograft rejection.
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PMID:Enhanced apoptosis of peripheral blood mononuclear cells in cardiac transplanted patients undergoing chronic immunosuppressive treatment. 1250 98

The possibility of immunotherapy for lymphoma by single FasL-Fas way was investigated. After pBillneo-mFasL was transformed into competent E. coli DH5alpha and amplified, the plasmid DNA was prepared and purified from the DH5alpha. To determine the primary structure and inserting direction of mFasL cDNA gene in pBillneo-mFasL, the plasmid DNA was cleaved by restriction enzyme, and the mFasL cDNA of pBillneo-mFasL was amplified by polymerase chain reaction (PCR), the DNA sequence of the PCR product was analysed by automatic DNA sequencing. After pBillneo-mFasL was transfected into COS-7 cells by liposome, the COS-7 cells were selected with G418 selective medium, and the expressing levels of mFasL cDNA on the COS-7 cell membrane was assayed by Western Blot. After the COS-7 cells higher expressing mFasL protein and mouse lymphoma cell line Yac-1 expressing Fas were cocultured for 5 hours, the suspending Yac-1 cells were collected and labeled by annexin V/PI kit. The apoptosis rate of the Yac-1 cells was tested by flow cytometry. The EcoRI cleaving products of pBillneo-mF asL included 920 bp and 7227 bp fragments. Its Hind III cleaving products included 1293 bp and 6807 bp fragments. These results showed: (1) the length of DNA sequence containing mFasL cDNA within pBillneo-mFasL is the same as theoretical length; (2) the inserting of mFasL cDNA in pBillneo-mFasL was in positive orientation. The expected 890 bp DNA fragments of mFasL cDNA (from ATG to +36 bp following TAA) emerged in PCR product with pBillneo-mFasL as a template. The sequencing result of the PCR product equaled the known mFasL cDNA sequence in the gene bank. The COS-7 cells transfected by pBillneo-mFasL and selected with G418 culture medium expressed more mFasL membrane protein assayed by Western Blot. After the COS-7 cells were cocultured with Fas(+) Yac-1 cells in different E:T ratios (1:1, 5:1 and 10:1) for 5 hours, the apoptosis rates of Yac-1 cells were (22 +/- 4.8)%, (32.18 +/- 7.8)%, and (51.8 +/- 5.4)%, respectively. These were obviously different from the control group (P < 0.01), in which the COS-7 cell was transfected by pBillneo (not carrying mFasL gene). It was concluded that lymphoma cells highly expressing Fas can be effectively killed through single Fas-FasL way in vitro.
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PMID:[Apoptosis of Fas(+) Yac-1 cells induced with Fas ligand-transfected COS-7 cells]. 1251 67

To determine whether the Fas receptor-Fas ligand (FasR-FasL) system, which triggers apoptosis in sensitive cells, is an important mechanism of cytotoxicity in myeloid leukemia. FasL expression was investigated in myeloid leukemia cells and its upregulation by a combination of IL-2 and INF-gamma, +/- as well as its function of inducing Jurkat cells to apoptosis mainly by flow cytometry (FCM). Results showed that leukemia cells expressed more FasL (3.59 +/- 1.05)% than that expressed in the healthy individuals (0.36% +/- 0.16)%, P < 0.001 and the FasL was upregulated (7.78 +/- 3.40)%, P < 0.01 when treated with IL-2 and IFN-gamma. Leukemia cells were co-cultivated with Jurkat cells for 24 hours. Then Jurkat cells were labeled with FITC-annexin V and PE-CD3 to assess apoptosis by FCM. The leukemia cells, which had been incubated with IL-2 and IFN-gamma, induced more Jurkat cells to apoptosis than the ones that freshly isolated from the peripheral blood mononuclear cells, which raised the figure from (8.28 +/- 1.61)% to (10.73 +/- 2.16%). And the supernatant derived from the former killed more Jurkat cells than the latter. It was concluded that human myeloid leukemia cells expressed high levels of functional FasL that can kill Jurkat T-cells by apoptosis. FasR-FasL sys tem could play a role in the "immune escape" and relapse of the leukemia. The induction of apoptosis through the Fas pathway might be a novel and effective approach for leukemia immunotherapy.
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PMID:[Study on expression and function of fas ligand in human myeloid leukemia cells]. 1251 81

Rapid leukemic cell kill at initial diagnosis of patients with acute lymphoblastic leukemia (ALL) has been shown to be associated with a favorable outcome. The aim of the present study was to investigate the effect of high dose methylprednisolone (HDMP) on in vivo blast cell apoptosis in children with ALL. Annexin V-binding and Fas (CD95), Fas ligand (FasL; CD95L), and Bcl-2 expression in PB blasts were determined in newly diagnosed children with ALL before and 4, 24, 96 h after initiation of HDMP treatment (n=20) or conventional dose steroids (CDS) (n=10) as the control group. A decrease in absolute blast count (from 40.8 x 09 to 21.4 x 109/l) associated with an increase in apoptosis (14.2 to 26.9%) (P < 0.05) was detected 4 h after initiation of HDMP. A significant increase in Fas and FasL expression was detected 96 h after HDMP. There was no significant change in apoptosis, Fas and FasL expression from baseline in the control group treated with CDS. The changes in Bcl-2 expression after treatment was not significant in both groups. The results of this preliminary study have shown that HDMP treatment was effective in inducing immediate (within 4 h) blast cell apoptosis. The contribution of Fas/FasL interaction in the rapid component of cell kill remains to be determined, as the increase in the expression of these molecules was evident later.
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PMID:The effects of high dose methylprednisolone on apoptosis in children with acute lymphoblastic leukemia. 1254 40

The effect of a variety of cell death-inducing reagents on the release of herpes simplex virus type 1 (HSV-1) was examined. Ionomycin was found to increase the release of HSV-1, whereas no significant increase was observed by the treatment with TNF-alpha, anti-Fas antibody, C2-ceramide, sphingosine, H-7, tyrphostin and camptothecin. Ionomycin induced an immediate early peak and a subsequent long-lasting elevation of intracellular Ca(2+) concentration ([Ca(2+)]i). In the absence of extracellular Ca(2+), ionomycin neither elevated [Ca(2+)]i nor increased the release of HSV-1 from the infected cells, indicating that Ca(2+) influx play an important role in the release of HSV-1. Studies with trypan blue and annexin V staining revealed that the ionomycin-induced alteration of [Ca(2+)]i was accompanied by cell death of the infected cells. Disintegration of cell membrane, cytoplasmic vacuole formation and the leakage of virus particles from the cell surface were observed by electron microscopy. These results indicate that Ca(2+)-dependent cell death showing necrotic alteration is responsible for the enhanced release of HSV-1. The data also give some initial insights into the functional importance of cell death during the late stages of HSV-1 infection.
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PMID:Effect of Ca2+-dependent cell death on the release of herpes simplex virus. 1255 89

The aim of this study was to look at the apoptosis of alveolar lymphocytes in hypersensitivity pneumonitis (HP). HP patients and normal unexposed controls were studied. The percentage of apoptotic lymphocytes was significantly lower in HP patients than in normal patients (37.4 +/- 3.4 versus 56.5 +/- 5.5% for Annexin V and propidium iodine detection methods and 0.4 +/- 0.1 versus 1.0 +/- 0.2% for dUTP nick end-labelling technique (TUNEL)). The proportion of bronchoalveolar lavage (BAL) lymphocytes positive for Fas antigen was significantly higher in HP patients than in normal subjects (71.7 +/- 5.4 versus 50.4 +/- 9.0%). However, no significant difference was found in the proportion of BAL lymphocytes positive for Fas ligand (FasL) between the two groups. Soluble Fas (sFas) levels in the BAL fluid of the patients and normals were 80.5 +/- 8.5 pg x mL(-1) and 23.2 +/- 3.1 pg x mL(-1), respectively. A positive correlation was found between the percentage of BAL lymphocytes and the levels of sFas for the total subjects but not within the separate study groups. The intracellular quantity of the inducible anti-apoptotic gene Bcl-xL product was significantly higher in the pulmonary lymphocytes of HP patients than in lymphocytes of the control, while no difference was found for constitutive anti-apoptotic protein (Bcl-2). In conclusion, the apoptosis of pulmonary lymphocytes is lower in hypersensitivity pneumonitis than in normal subjects. This could be explained, at least in part, by an increase of soluble Fas, the anti-apoptic gene, and Bcl-xL.
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PMID:Apoptosis of bronchoalveolar lavage lymphocytes in hypersensitivity pneumonitis. 1260 34

Activation-induced cell death (AICD) is a phenomenon in which activated T cells undergo apoptosis upon restimulation. We are studying a form of AICD that can occur before cells become competent to die by Fas (hence "early" AICD) and which depends on the presence of perforin. Previous studies indicate that it does not occur through granule exocytosis but via some endogenous pathway. We here investigate a possible role for caspases. Caspase 3(-/-) cells were protected, suggesting a role for caspase 3 in early AICD. After recrosslinking, caspase 3 activity could be detected in cell lysates between 3 and 12 h, and CD8(+) T cells became annexin V-positive between 15 and 18 h. Blocking anti-Fas ligand antibody failed to inhibit death, and no processing of either caspase 8 or caspase 9 was detected in recrosslinked cells. Furthermore, T cells lacking functional caspase 9 continued to die in early AICD. Thus, perforin-dependent early AICD appears to require activation of caspase 3, but not caspases 8 or 9. As perforin has no intrinsic catalytic abilities, we propose that it releases some endogenous activity that can activate caspase 3.
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PMID:Perforin-dependent activation-induced cell death acts through caspase 3 but not through caspases 8 or 9. 1261 97

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