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)

MRL/Mp +/+ (MRL/+) mice, not bearing the lpr gene, are known to have age-related autoimmune lesions in several organs such as pancreas, salivary and lacrimal glands at 30-weeks-old or more. In this study, MRL/+ mice were ovariectomized at 4-weeks-old, and their natural histories were analysed. Ovariectomy (Ovx) of MRL/+ mice led to marked acceleration of organ-specific autoimmune lesions exclusively in the salivary and lacrimal glands at 8-weeks-old or more, whereas no significant inflammatory change was observed in the pancreas. In the vast majority of inflammatory infiltrates, CD3+ CD4+ T cells were predominant in both the salivary and lacrimal glands of Ovx-MRL/+ mice. Up-regulated expression of cytokine genes including IL-1 beta, TNF-alpha, IL-2, interferon (IFN)-gamma, and IL-6 was detected in the salivary gland of Ovx-MRL/+ mice by reverse transcriptase (RT)-PCR analysis. FACS analysis of spleen cells of Ovx-mice revealed increase in I-Ak expression on B220+ cells, and autoantibody production against the salivary gland-specific antigen in sera from Ovx-MRL/+ mice, but not in control mice. These results suggest that age-related autoimmunity in the salivary and lacrimal glands were accelerated in Ovx-MRL/+ mice, and that autoreactive Th1 cells were activated associated with organ-specific autoantibody production.
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PMID:Accelerated onset of age-related autoimmune lesions in MRL/+ mice by ovariectomy. 908 79

Numerous cytokines induce symptoms characteristic of the flu syndrome common to acute viral infections. To better characterize the cytokine mRNA profile associated with the early phase of this syndrome, we examined the induction of cytokine mRNAs in spleens of mice 1, 2, and 4 h following intraperitoneal inoculation of Newcastle disease virus (NDV). The reverse transcriptase-polymerase chain reaction was used to detect mRNAs for mouse proinflammatory cytokines [interleukin (IL)-1 alpha, IL-1 beta, IL-6, tumor necrosis factor-alpha (TNF-alpha), macrophage colony-stimulating factor (M-CSF), and interferon (IFN)-gamma] and type I IFNs (IFN-alpha 4 and IFN-beta). We observed a rapid (within 2 h) induction of most of these cytokine mRNAs in the mouse spleen following challenge with live NDV or the viral stimulant poly[rI:rC]. IL-1 beta, M-CSF, and IFN-gamma mRNAs were also induced by heat-inactivated NDV, suggesting the possibility of endotoxin contamination of the virus (confirmed by Limulus lysate assay). Examination of cytokine induction by comparable doses of lipopolysaccharide indicated that endotoxin contamination could account for the cytokine mRNA-inducing activity of the heat-inactivated virus. These studies point to a critical control (heat-inactivated virus) for viral cytokine studies. In addition, they indicate that certain cytokine mRNAs (IL-1 alpha, IL-6, M-CSF, IFN-gamma, IFN-alpha, and IFN-beta) are rapidly induced in the spleen when live virus is inoculated intraperitoneally, independently of contaminating endotoxin.
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PMID:Early induction of proinflammatory cytokine and type I interferon mRNAs following Newcastle disease virus, poly [rI:rC], or low-dose LPS challenge of the mouse. 914 48

Cytokine gene expression was examined by qualitative and semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) in the lungs of Mycoplasma pneumoniae infected immune C57BL/6 mice depleted of either CD4+, CD8+ or both CD4+ and CD8+ T cells. Immediately after M. pneumoniae reinfection of control immune mice, mRNAs for TNF-alpha, IFN-gamma, IL-1 beta, IL-6, IL-2 and IL-2 receptor were promptly detected in the lungs. In animals depleted of CD4+ T cells, mRNA expression for IL-2, IL-2 receptor and IFN-gamma were completely abrogated and mRNA expression for TNF-alpha, IL-1 beta and IL-6 were reduced by 10- to 100-fold. In mice depleted of CD8+ T cells, mRNA expression for IL-2 and the IL-2 receptor was also undetectable, while mRNA for TNF-alpha, IL-1 beta and IL-6 were only marginally decreased. Histological evaluation of the infected lungs performed in parallel revealed dense mononuclear infiltrations around small bronchi and small blood vessels in control reinfected mice. In contrast, in CD4+ T cell-depleted mice, these focal accumulation of lung tissue infiltrating cells were found to be greatly reduced. The data indicate that the inflammatory response in lung tissue thought to be mainly responsible for Mycoplasma pneumoniae disease is associated with an increased level and a prolonged expression of proinflammatory cytokines due to CD4+ lung infiltrating T cells.
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PMID:Cytokine gene expression in immune mice reinfected with Mycoplasma pneumoniae: the role of T cell subsets in aggravating the inflammatory response. 914 34

It has been reported that the mRNA of the type 1 cytokine, interferon-gamma (IFN-gamma)--but not the type 2 cytokine interleukin-4 (IL-4)--is detected in synovial tissues of rheumatoid arthritis (RA) patients, whereas both IFN-gamma and IL-4 mRNA are detected in reactive arthritis (ReA). To evaluate such data more extensively, we obtained 208 synovial specimens in a prospective study of 52 early synovitis patients (13 RA, 11 ReA, 28 undifferentiated oligoarthropathy) and analyzed type 1 and type 2 cytokine mRNA expression in specimens containing sufficient mRNA. Using a nested reverse transcriptase polymerase chain reaction technique, we measured the relative mRNA levels of 10 cytokines and CD3 delta chain. We detected IL-10, IL-15, and CD3 delta chain mRNA in all RA and ReA patients and frequently detected tumor necrosis factor-alpha, IL-1 beta, and IFN-gamma mRNA. IL-6 and IL-12 p40 mRNA were detected in approximately one-half of the patients. We also detected greater amounts of IL-2 and IFN-gamma mRNA in ReA than were detected in RA. However, we rarely detected IL-4 or IL-13 mRNA. Similar cytokine profiles were observed in undifferentiated oligoarthropathy. The amounts of cytokine mRNAs, except for IL-10, in specimens from the patients taking prednisone or second-line antirheumatic drugs tended to be less than in specimens from the patients taking neither prednisone nor second-line antirheumatic drugs. These results suggest that cytokine mRNA profiles in patients with RA, ReA, and undifferentiated arthritis in their early stages are skewed toward proinflammatory macrophage-derived and type 1 cytokines. IL-10--not IL-4 or IL-13--mRNA appears to be the major antiinflammatory cytokine mRNA. Drug therapy is associated with depressed proinflammatory and type 1 cytokine mRNA production. The differences in the expression of IL-2 and IFN-gamma mRNA between RA and ReA may reflect unique etiological or host factors associated with the early stages of these diseases.
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PMID:In vivo gene expression of type 1 and type 2 cytokines in synovial tissues from patients in early stages of rheumatoid, reactive, and undifferentiated arthritis. 915 45

The product of the protooncogene c-kit is the receptor for the hematopoietic cytokine stem cell factor (SCF). C-kit is expressed on leukemic cells of the erythroid, myeloid, and mast-cell lineage and SCF has a proliferative effect on some of these cells. The role of SCF and c-kit in lymphoid malignancies is much less clear. Here we review the role of c-kit in normal lymphopoiesis and summarize its role in lymphoid malignancies. C-kit is expressed in normal lymphopoiesis and its ligand SCF synergizes with IL-7 to enhance the proliferation of B- and T-cell progenitors. In malignant lymphopoiesis, c-kit can also be expressed in B and T-lymphoblastic cells from children with non Hodgkin's lymphoma (NHL) or acute lymphoblastic leukemia (ALL) when analyzed by the highly sensitive reverse transcriptase polymerase chain reaction (RT-PCR). While c-kit receptors were detected by flow cytometric (FCM) analysis on about 40% of fresh T-lymphoblastic biopsy tumor cell preparations or T-lymphoblastic cell lines, no receptors were detected on B-lymphoblastic fresh cells or cell lines from children with B-ALL or Burkitt's lymphoma (BL). Almost all of the lymphoblastic cells expressing c-kit protein responded to recombinant human (rh)SCF with a downregulation of c-kit receptors. A proliferative response was detected only in a minority of these cells. B-ALL or BL cell lines showed no response to rhSCF. Upregulation of c-kit in T-lymphoblastic cells could be demonstrated by the addition of IL-1 beta, TNF-alpha, TGF-beta or A23187, and downregulation by rhSCF or phorbol myristate acetate (PMA). Despite upregulation of c-kit mRNA, protein remained undetectable on B-ALL or BL cells in the presence of A23187. The metabolic state of the cells seemed to influence c-kit expression, since c-kit was upregulated in T-lymphoblastic cells by the addition of new medium. C-kit appears to play a role in the growth of some malignant T-lymphoblastic but not B-lymphoblastic cells.
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PMID:C-kit receptors in childhood malignant lymphoblastic cells. 916 31

Our previous reports demonstrated the concomitant release of IL-1 beta and IL-1 inhibitory activity in the culture supernatants of BALF macrophages in both healthy subjects and patients with interstitial lung diseases. IL-1 inhibitory activities decreased in healthy smokers (HS), and patients with sarcoidosis (Sar), or idiopathic pulmonary fibrosis (IPF), compared with those in healthy nonsmokers (HNS), though an increase in IL-1 beta release was not detected. IL-1 inhibitory activity was mainly characterized as IL-1 receptor antagonist (IL-1ra). In this study, we confirmed a decrease in IL-1ra in terms of the amounts of protein (enzyme-linked immunoassay) and gene transcripts (reverse transcriptase polymerase chain reaction followed by high performance liquid chromatography). Imbalance between IL-1ra and IL-1 beta was expressed as a molar ratio of IL-1ra/IL-1 beta protein: (Sar; 4.20 +/- 2.06, IPF; 4.26 +/- 3.41, HS; 3.44 +/- 3.09 versus NS 8.33 +/- 2.77: P < 0.001). These results were similar in terms of the amounts of gene transcripts. In conclusion, the imbalance of IL-1 beta and IL-1ra production was confirmed at three levels: biological activity, amounts of protein, and gene transcript obtained from BALF macrophages in chronic inflammatory processes in the lungs.
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PMID:Quantitative evaluation of the IL-1 beta and IL-1 receptor antagonist obtained from BALF macrophages in patients with interstitial lung diseases. 918 88

Macrophages and polymorphonuclear cells (PMN) play a major role as cells primarily responsive to microbial biological response modifiers (BRM). Although much attention has been given to macrophages, PMN have been relatively underinvestigated. We have recently studied the responses of PMN from HIV- and HIV+ subjects after stimulation with a powerful immunomodulatory fraction from the cell wall of Candida albicans (MP-F2) and compared this to bacterial lipopolysaccharide (LPS). Both cytokine patterns and PMN anticandidal activity were investigated. MP-F2, like LPS, was an active inducer of interleukin-8 (IL-8), tumor necrosis factor alpha (TNF-alpha), IL-6, and IL-1 beta production by PMN and monocytes from all subjects. IL-12 was also produced by MP-F2-stimulated PMN in the presence of interferon-gamma (IFN-gamma). PMN from HIV+ subjects showed increased in vitro expression of TNF-alpha and IL-6 genes as determined by semiquantitative reverse transcriptase-polymerase chain reaction. In all subjects, cytokine gene expression was strongly stimulated by MP-F2 or LPS and inhibited by IL-10. Production of IL-6 and TNF-alpha protein (measured by ELISA) was higher in PMN from HIV+ subjects in at least one of the conditions tested (unstimulated or stimulated by LPS or MP-F2). However, the amount of the C-X-C chemokine IL-8 was equal in PMN from HIV- and HIV+ subjects. PMN from HIV+ subjects were at least as active in inhibiting candide growth as PMN from HIV- controls. In both groups PMN were equally stimulated by MP-F2 and LPS. Only in severely neutropenic subjects was there some reduction in the anticandidal activity but not in cytokine responses. When appropriately stimulated by microbial BRM, PMN are active producers of pro-inflammatory and immunomodulatory cytokines. This production is not only totally preserved in HIV+ subjects but may be higher than in PMN from HIV- subjects and may be coupled with an efficient anticandida activity. We suggest that during common bacterial or fungal infections PMN may contribute to the dysregulated production of inflammatory cytokines in AIDS patients.
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PMID:Possible participation of polymorphonuclear cells stimulated by microbial immunomodulators in the dysregulated cytokine patterns of AIDS patients. 922 94

Multinucleated giant cells (MGCs) are a key feature of granulomas. They have been studied with respect to the mechanism and regulation of their formation, but the function of these cells still remains elusive. A new method for the in vitro generation of granulomas was developed and characterized in which L3 larvae of Nippostrongylus brasiliensis, as a target for the cellular response, were co-incubated with human mononuclear blood cells. The development of epithelioid cells and MGCs was observed and single isolated MGCs were analysed by the reverse transcriptase polymerase chain reaction method. The presence of tumour necrosis factor alpha (TNF alpha), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and inducible nitric oxide synthase (iNOS) transcripts in MGCs was demonstrated. It is proposed that MGCs in the granuloma model may in part represent an active cellular constituent involved in granuloma formation and turnover and in the destruction of the irritant.
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PMID:Properties of multinucleated giant cells in a new in vitro model for human granuloma formation. 922 48

The interleukin-1 (IL-1) system has been shown to play an important role in human and murine embryo implantation. Recent studies have documented immunohistochemical evidence of interleukin-1 beta (IL--1 beta), interleukin-1 receptor antagonist (IL-1ra) and interleukin-1 receptor type I (IL-1R tI) in human preimplantation embryos and protein levels of interleukin-1 alpha (IL-1 alpha), IL-1 beta and IL1ra in human preimplantation embryo culture fluid have been correlated with successful implantation and pregnancy. Our aim in this study was to detect IL-1 beta, Il-1ra and Il-1R tI mRNA in single preimplantation mouse embryos and to describe the frequency of positive mRNA-expression at different developmental stages. B6C3F1-mice, 12 weeks old were pregnant mare serum gonadotropin (PMSG)/human chorionic gonadotropin (hCG)-stimulated and mated. Animals were sacrificed at day 0.5, and zygotes were flushed from the tubes and cultured in HAMs-F10 medium. 2-cell- (2C-), 8-cell- (8C-), morula- (M-), early blastocyst- (EB-) and hatching blastocyst- (HB-) stage embryos were examined by one round of reverse transcriptase (RT) followed by two rounds of polymerase chain reaction (PCR) carried out on individual mouse embryos for beta-actin (internal standard), IL-1 beta, IL-1ra and IL-1R tI-mRNAs. The frequencies of positive mRNA-expressions were as follows (2C/8C/M/EB/HB); beta-actin: 91/96/100/100/98%; IL-1b: 0/0/2.5/6.25/19; IL-1ra; 0/5/30/41/74% and IL-1R tI: 0/0/10/20/25%. The incidence of IL-1ra mRNA expression increased with developmental stage. IL-1ra mRNA seems to be expressed in a very high percentage (74%) of embryos near the time of implantation, whereas the percentage of IL-1 beta-mRNA positive embryos is surprisingly low (19%).
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PMID:Different pattern of interleukin-1 beta-(IL-1 beta), interleukin-1 receptor antagonist- (IL-1ra) and interleukin-1 receptor type I- (IL-1R tI) mRNA-expression in single preimplantation mouse embryos at various developmental stages. 929 78

IL-1 beta converting enzyme (ICE), a proteolytic enzyme that converts the inactive precursor of interleukin-1 beta (IL-1 beta) to its mature active form, has been abundantly detected in the IL-1 beta producing cells in the spleen. Since IL-1 beta is a potent neuro-endocrine-immuno modulator, alterations in the production of IL-1 beta by an exogenous factor, such as morphine or ethanol, may have deleterious effects on the system as a whole. In this study, we examined the expression of ICE in the spleens of rats given chronic treatment with morphine versus ethanol using reverse transcriptase-polymerase chain reaction (RT-PCR). The expression of ICE in the spleen of rats given chronic morphine was clearly less than that of the animals given placebo, however, it was similar for both rats on ethanol and control diets. These data suggest that chronic use of morphine, but not ethanol, attenuates the expression of ICE in the spleen.
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PMID:Chronic exposure to morphine, but not ethanol, attenuates the expression of interleukin-1 beta converting enzyme in rat spleen. 929 96


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