Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using a cell sorter, CD16-CD56bright natural killer (NK) cells were sorted from decidual mononuclear cells at an early stage of pregnancy. These cells were examined by the reverse transcriptase-polymerase chain reaction (RT-PCR) method for their expression of mRNA coding for the following 12 cytokines: IL-1 beta, IL-2, IL-3, IL-4, IL-5, IL-6, granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), macrophage colony-stimulating factor (M-CSF), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), and leukemia inhibitory factor (LIF). Although mRNA coding for every cytokine was detected in decidual mononuclear cells, mRNAs coding for only G-CSF, GM-CSF, M-CSF, TNF-alpha, IFN-gamma, and LIF were detected in CD16-CD56bright NK cells. Also, the supernatant of CD16-CD56bright NK cell cultures was found to contain G-CSF, GM-CSF, M-CSF, TNF-alpha, IFN-gamma, and LIF. These findings indicate that CD16-CD56bright NK cells produce many different cytokines and that these cytokines may play an important role in a successful pregnancy.
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PMID:Cytokine production by CD16-CD56bright natural killer cells in the human early pregnancy decidua. 768 93

The c-myb protooncogene plays a major role in regulating the process of in vitro and in vivo hematopoiesis via its activity as transcriptional regulator in hematopoietic progenitor cells. Since the bone marrow microenvironment appears to regulate in vivo hematopoiesis by maintaining the growth of multipotent progenitors via secretion of specific cytokines, we asked whether c-myb is also required for the proliferation of and/or cytokine production by stromal cells that generate fibroblast-like colonies (fibroblast colony-forming units [CFU-F]). Using the reverse transcriptase polymerase chain reaction technique, we detected low levels of c-myb mRNA transcripts in human normal bone marrow fibroblasts. Treatment of these cells with c-myb antisense oligodeoxynucleotides caused downregulation of c-myb expression, decreased in the number of marrow CFU-F colonies (approximately 54% inhibition) and in the cell number within residual colonies (approximately 80%), and downregulation of granulocyte/macrophage colony-stimulating factor (GM-CSF) and stem cell factor (SCF) mRNA expression. Transfection of T98G glioblastoma cells, in which expression of c-myb, GM-CSF, and SCF mRNAs is undetectable or barely detectable, with a plasmid containing a full-length c-myb cDNA under the control of the SV40 promoter induced the expression of biologically active SCF and GM-CSF in these cells. Regulation of GM-CSF expression by c-myb was due in part to transactivation of the GM-CSF promoter. These results indicate that, in addition to regulating hematopoietic cell proliferation, c-myb is also required for proliferation of and cytokines synthesis by bone marrow fibroblasts.
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PMID:Regulation of proliferation and cytokine expression of bone marrow fibroblasts: role of c-myb. 768 94

As an approach for characterizing the molecules involved in the proliferation and differentiation of hematopoietic stem cells we have compared the ability of four murine stromal cell lines, MS-5, MS-K, both derived from Dexter cultures, BMS1 and BMS2 both derived from Whitlock-Witte cultures, to sustain murine long term hematopoiesis and to express the major hematopoietic cytokine genes. As opposed to the three other cell lines, MS-5 supports the maintenance of stem cells for up to 4-5 weeks. However, reconstituting stem cell output was reduced while clonogenic cell (day 12 and day 8 spleen colony-forming units, granulo-macrophagic, and erythroid progenitor cells) output was markedly increased. This hematopoietic-promoting activity is at least in part mediated by soluble molecules since medium conditioned with MS-5 cells was able to partially complement the nonsupportive cell line BMS1. The comparative study of the cytokine gene expression in MS-5 and in the nonsupportive cell lines included Northern blot and reverse transcriptase-polymerase chain reaction analysis of messenger RNA for interleukin-1, -3, -6, granulo-macrophage-colony-stimulating factor (GM-CSF), granulocyte-CSF, macrophage-CSF, stem cell factor, transforming growth factor-beta, tumor necrosis factor-alpha, macrophage inflammatory protein-1 alpha, and leukemia inhibitory factor. None of these molecules or their association were found to clearly confer to the MS-5 cell line its hematopoietic-promoting activity raising the possibility that uncharacterized molecule(s) would be involved in the proliferation and differentiation of stem cells.
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PMID:Hematopoietic-promoting activity of the murine stromal cell line MS-5 is not related to the expression of the major hematopoietic cytokines. 770 74

Plasma cell granuloma (PCG) is a pseudotumor of unknown origin. It is frequently accompanied by acute-phase clinical and biological signs that resume after complete surgical removal, suggesting production of soluble mediators. We therefore investigated the role of cytokines in a previously healthy 10-year-old boy with a PCG of the lung and systemic symptoms. In this case, very high serum levels of interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) were found before tumor excision, associated with inflammatory signs including major hyper-gamma-globulinemia. Pathologic analysis of the tumor showed an accumulation of fibroblasts and plasma cells producing immunoglobulins. Local production of IL-1 beta and IL-6 could be demonstrated at the messenger RNA (mRNA) level by the reverse transcriptase polymerase chain reaction and could be attributed to inflammatory cells by in situ hybridization and immunohistochemistry, whereas plasma cells exhibited membrane expression of the IL-6 receptor. Postsurgery follow-up showed rapid normalization of serum IL-1 beta and IL-6, whereas inflammatory protein levels decreased. This confirms the local production of cytokine within the PCG and raises the question of whether a dysregulation of cytokine production initiates the disease.
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PMID:Interleukin-6 and interleukin-1 beta production in a pediatric plasma cell granuloma of the lung. 772 69

Expression of the IL-13 gene in malignant tissues from 26 human B-cell lymphoid malignancies was analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR). A positive signal was detected in 16 cases, which included high grade B lymphomas, follicular lymphomas and B-cell chronic lymphocytic leukemias. IL-13 mRNA was also detected in the 9 malignant B cell lines and in the 6 lymphoblastoid cell lines tested, as well as in freshly isolated malignant B cells from 2 patients with a Burkitt's lymphoma. Two of 8 T-cell lymphomas and 2 of 4 T-cell lines expressed the IL-13 gene. In contrast, IL-13 gene expression was not detected in any of the 5 non-lymphoid cell lines tested. No specific binding of radiolabeled IL-13 was detected on B cell lines, suggesting an absence of IL-13 receptors on such cells. This conclusion was also supported by the inability of IL-13 or anti-IL-13 antibodies to affect the growth of malignant B cells. Taken together, these results show that both malignant and EBV-transformed B lymphocytes, either freshly isolated or maintained as cell lines, express the IL-13 gene. This raises the question of the role of B lymphocyte-derived IL-13, a B lymphocyte stimulating cytokine, on the in vivo function of normal B lymphocytes as well as on the in vivo behaviour of B lymphoid malignancies.
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PMID:Interleukin-13 gene expression by malignant and EBV-transformed human B lymphocytes. 772 91

An involvement of cellular immunity in alveolar echinococcosis is strongly suggested by the intense granulomatous infiltrations observed around the hepatic parasite lesions. However, the basis of cellular immunoregulation in patient with alveolar echinococcosis is poorly understood. The present report shows a comparative analysis of lymphoid cell function in peripheral blood mononuclear cells (PBMC) of 16 patients with alveolar echinococcosis and of healthy individuals. Our in vitro restimulation studies with crude Echinococcus multilocularis antigen demonstrated that PBMC from patients with alveolar echinococcosis were responsive to challenge with parasitic antigen as measured by lymphoid cell proliferation. In this system, we also evaluated cytokine expression at the gene and protein levels after stimulation with E. multilocularis antigen. Analysis of cytokine mRNA expression revealed distinct patterns of cytokine expression in patients and normal donors. By using reverse transcriptase PCR, we could demonstrate that the TH1 cytokine transcripts interleukin-2 (IL-2) and gamma interferon (IFN-gamma) are present in PBMC from patients with alveolar echinococcosis. Moreover, it was found that stimulation with E. multilocularis antigen induced or enhanced the expression of the TH2 cytokine IL-3, IL-4, IL-10, and especially IL-5 mRNAs in PBMC from 13 of 16 patients with alveolar echinococcosis. Two patients who were examined after radical surgery, as well as another patient with a stable course of the disease under continuous chemotherapy, were not able to generate the same pattern of cytokine response and had no evidence of IL-5 mRNA synthesis. In contrast to the frequent expression of TH2 cytokine mRNAs observed in patients with alveolar echinococcosis, PBMC cultures from normal donors showed prominent IL-2 and IFN-gamma mRNA expression but weak IL-3, IL-4, and IL-10 mRNA expression. Most interestingly, IL-5 mRNA was substantially absent in PBMC from healthy individuals. In accordance with the mRNA studies, it was found that E. multilocularis antigen induced the secretion of large amounts of IL-5 and intermediate amounts of IFN-gamma in patients with alveolar echinococcosis, whereas large amounts of IFN-gamma and no or threshold amounts of IL-5 were detected in supernatants from healthy individuals. Collectively, the present study provides the first evidence that a TH2 immune response is gradually activated during the course of E. multilocularis infection, indicating a critical role for IL-5 in the manifestation of human alveolar echinococcosis.
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PMID:Interleukin-5 is the predominant cytokine produced by peripheral blood mononuclear cells in alveolar echinococcosis. 772 73

Airway inflammation is characterized by leukocyte extravasation around the peribronchial mucosa and into the airway of the lung. In the present study we utilized a model of airway inflammation induced by intratracheal challenge with soluble parasite (Schistosoma mansoni) egg Ag (SEA) in presensitized mice. The subsequent inflammatory response and leukocyte recruitment consists of early neutrophil (8 to 24 h) and later eosinophil (48 to 72 h) infiltration into the interstitium and airway. Little neutrophil and no eosinophil recruitment was observed in presensitized control mice challenged with vehicle. Multiple studies have demonstrated a crucial role for TNF-alpha during inflammatory responses. In these experiments we investigated the role of TNF-alpha in Ag-specific eosinophilic airway inflammation. Measurement of TNF-alpha expression by reverse transcriptase-PCR and ELISA in whole lung homogenates of SEA-challenged mice demonstrated an early increase in TNF-alpha levels (1 to 8 h). To determine the specific role of TNF-alpha in leukocyte recruitment during airway inflammation, mice were treated with soluble TNF-alpha receptor linked to an Fc Ab molecule (sTNFr-:Fc). This treatment has previously been used to effectively neutralize TNF in vivo. Intratracheal SEA-challenged mice treated with sTNFr-FC demonstrated significantly decreased leukocyte recruitment into the lung and airway. The inflammatory response in the lungs in sTNFr-Fc-treated mice was significantly decreased throughout the study period, as compared with control mice. An approximate decrease in early neutrophil infiltration into the airway was observed when sTNFr-Fc was administered 2 h before the Ag challenge. Eosinophil infiltration was also diminished when sTNFr-Fc was administered before Ag challenge. Interestingly, when sTNFr-Fc was administered therapeutically 24 h after Ag challenge, the eosinophil response was nearly abrogated at 48 h after challenge. These studies indicate that TNF-alpha acts as an initial inflammatory cytokine that subsequently regulates both early neutrophil infiltration and eosinophil recruitment into the lung and airspace.
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PMID:TNF-alpha mediates recruitment of neutrophils and eosinophils during airway inflammation. 773 Jun 42

A previous study reported the increased expression of the cytokine TNF in the adipose tissue of genetically obese rodents. To examine this paradigm in humans, we studied TNF expression in lean, obese, and reduced-obese human subjects. TNF mRNA was demonstrated in human adipocytes and adipose tissue by Northern blotting and PCR. TNF protein was quantitated by Western blotting and ELISA in both adipose tissue and the medium surrounding adipose tissue. Using quantitative reverse transcriptase PCR (RT-PCR), TNF mRNA levels were examined in the adipose tissue of 39 nondiabetic subjects, spanning a broad range of body mass index (BMI). There was a significant increase in adipose TNF mRNA levels with increasing adiposity. There was a significant correlation between TNF mRNA and percent body fat (r = 0.46, P < 0.05, n = 23). TNF mRNA tended to decrease in very obese subjects, but when subjects with a BMI > 45 kg/m2 were excluded, there was a significant correlation between TNF mRNA and BMI (r = 0.37, P < 0.05, n = 32). In addition, there was a significant decrease in adipose TNF with weight loss. In 11 obese subjects who lost between 14 and 66 kg (mean 34.7 kg, or 26.6% of initial weight), TNF mRNA levels decreased to 58% of initial levels after weight loss (P < 0.005), and TNF protein decreased to 46% of initial levels (P < 0.02). TNF is known to inhibit LPL activity. When fasting adipose LPL activity was measured in these subjects, there was a significant inverse relationship between TNF expression and LPL activity (r = -0.39, P < 0.02, n = 39). With weight loss, LPL activity increased to 411% of initial levels. However, the magnitude of the increase in LPL did not correlate with the decrease in TNF. Thus, TNF is expressed in human adipocytes. TNF is elevated in most obese subjects and is decreased by weight loss. In addition, there is an inverse relationship between TNF and LPL expression. These data suggest that endogenous TNF expression in adipose tissue may help limit obesity in some subjects, perhaps by increasing insulin resistance and decreasing LPL.
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PMID:The expression of tumor necrosis factor in human adipose tissue. Regulation by obesity, weight loss, and relationship to lipoprotein lipase. 773 78

The pro-inflammatory molecules, tumor necrosis factor alpha (TNF alpha), interleukin 1 (IL-1), interleukin 6 (IL-6), and prostaglandin E2 (PGE2), are postulated to have a role in human pregnancy and parturition. The ability of interleukin 4 (IL-4) to suppress the production of TNF alpha, IL-1, IL-6, and PGE2 by activated monocytes prompted us to investigate a possible regulatory role for IL-4 in human gestation. Immunohistochemical techniques were used to show that human amnion epithelium stained positively for IL-4. Tissue from both the first (n = 5) and third (n = 46) trimester expressed immunoreactive IL-4, which was detected by the use of four antihuman IL-4 monoclonal antibodies. Analysis of mRNA by reverse transcriptase-polymerase chain reaction (RT-PCR) on RNA extracts of amnion epithelial cells indicated that they were the source of IL-4. One of the anti-IL-4 antibodies used stained IL-4 protein associated with the basement membrane of the amnion epithelium. The mechanism of this association was investigated. IL-4 was shown to be a heparin-binding cytokine, which would enable it to bind to components of the extracellular matrix. Thus, this study identified a previously undescribed cellular source of IL-4, implicating a role for IL-4 in human gestation. Additionally, glycosaminoglycan binding may regulate IL-4 activity in vivo.
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PMID:Interleukin 4 production by human amnion epithelial cells and regulation of its activity by glycosaminoglycan binding. 778 6

When administered as single agents, both interferon gamma (IFN-gamma) and interleukin 6 (IL-6) significantly increase carcinoembryonic antigen (CEA) and HLA class I antigen expression on the surface of human colorectal tumour cells. Studies were carried out to determine whether by combining those cytokines a synergistic enhancement of CEA and HLA expression could result. The findings revealed that the administration of 20 units IFN-gamma along with 1.7 ng IL-6, concentrations of each cytokine that individually induced minimal antigenic changes, together synergistically increased CEA and HLA class I as well as induced qualitative changes in HLA expression on WiDr human colon carcinoma cells. The magnitude of the synergistic increases in CEA and HLA class I expression were reminiscent of the level of antigen augmentation observed when administering 20- to 100-fold higher amounts of each cytokine as a single agent. Also, the addition of IL-6 potentiated the IFN-gamma induction of HLA class II expression. The combined administration of IL-6 potentiated the IFN-gamma did not have any additive or synergistic effects on the growth suppression of those tumour cells. Interestingly, utilization of specific neutralizing antibodies for type I interferons abrogated the increases of CEA and HLA expression seen with IL-6 treatment alone or in combination with IFN-gamma. Moreover, reverse transcriptase/polymerase chain reaction analyses revealed a constitutive expression as well as a temporal increase of IFN-beta mRNA transcripts in colon tumour cells treated with IL-6. Therefore, the findings provide indirect evidence that IFN-beta production seems to play a critical role in the ability of IL-6 to upregulate antigen expression alone or in combination with IFN-gamma. These findings provide insight into cytokine combinations that synergistically upregulate tumour-associated and normal HLA antigen expression on the surface of human tumour cells. Those results provide the rationale for the combined use of such cytokines to heighten tumour cell recognition in monoclonal antibody- or cell-mediated-based immunotherapeutic approaches.
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PMID:Synergistic effects of IL-6 and IFN-gamma on carcinoembryonic antigen (CEA) and HLA expression by human colorectal carcinoma cells: role for endogenous IFN-beta. 778 31


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