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)

In order to better understand the immunoregulation following Mycobacterium tuberculosis infection, cytokine mRNA induction in response to in vitro infection of human monocytes with live virulent M. tuberculosis H37Rv cocultured with autologous lymphocytes was quantitated by reverse transcriptase-PCR. Induced levels of interleukin 1 beta (IL-1 beta), IL-2, tumor necrosis factor alpha, and gamma interferon (IFN-gamma) were compared among groups of individuals representing three phases of immunity to infection with M. tuberculosis: naive normal control subjects, purified protein derivative (PPD)-reactive normal donors, and individuals with active tuberculosis (TB [diseased]). Levels of IL-1 beta and tumor necrosis factor alpha mRNA in cocultured cells from TB patients were 51 and 45%, respectively, of those obtained in cells from sensitized healthy volunteers and were comparable to those from naive normal donors. Lymphoproliferative responses to M. tuberculosis and induction of the T-cell cytokine IL-2 were predictably high in the cells of PPD-sensitized donors, low in normal naive individuals, and variable among TB patients. In contrast, the induced level of another lymphokine, IFN-gamma, did not follow the pattern seen in IL-2 induction. Infection with live M. tuberculosis induced high levels of IFN-gamma mRNA in lymphocytes of both PPD-sensitized and normal naive donors compared with those of TB patients. Interestingly, polyclonal stimulation with the mitogen concanavalin A induced similar IFN-gamma levels in cells from all three donor groups. The high level of IFN-gamma induced by the infection of monocytes from naive normal donors suggests a role for natural killer (NK) cells in the production of IFN-gamma in this coculture system. This response appears independent of the role performed by T cells.
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PMID:Cytokine gene expression by cultures of human lymphocytes with autologous Mycobacterium tuberculosis-infected monocytes. 813 51

Among a group of 70 individuals who met the criteria established by the Centers for Disease Control and Prevention (Atlanta) for chronic fatigue syndrome (CFS), 12%-28% had serum levels exceeding 95% of control values for tumor necrosis factor (TNF) alpha, TNF-beta, interleukin (IL) 1 alpha, IL-2, soluble IL-2 receptor (sIL-2R), or neopterin; overall, 60% of patients had elevated levels of one or more of the nine soluble immune mediators tested. Nevertheless, only the distributions for circulating levels of TNF-alpha and TNF-beta differed significantly in the two populations. In patients with CFS--but not in controls--serum levels of TNF-alpha, IL-1 alpha, IL-4, and sIL-2R correlated significantly with one another and (in the 10 cases analyzed) with relative amounts (as compared to beta-globin or beta-actin) of the only mRNAs detectable by reverse transcriptase-coupled polymerase chain reaction in peripheral-blood mononuclear cells: TNF-beta, unspliced and spliced; IL-1 beta, lymphocyte fraction; and IL-6 (in order of appearance). These findings point to polycellular activation and may be relevant to the etiology and nosology of CFS.
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PMID:Dysregulated expression of tumor necrosis factor in chronic fatigue syndrome: interrelations with cellular sources and patterns of soluble immune mediator expression. 814 43

Using reverse transcriptase-linked polymerase chain reaction, the effect of polycyclic aromatic hydrocarbons (PAHs) on IL-1 alpha, IL-1 beta and IL-6 gene expression in cultured human keratinocytes was studied. Exposure to beta-naphthoflavone and benz(a)anthracene resulted in a higher copy number of IL-1 alpha and IL-6 mRNA while lower level of IL-1 beta mRNA was detected in these cells. These data suggest that, like ultraviolet B (UVB) radiation, ubiquitous environmental carcinogenic PAHs are potent inducers of IL-1 alpha and IL-6 cytokines and, unlike UVB, they downregulate IL-1 beta in human keratinocytes.
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PMID:Chemical carcinogens increase IL-1 alpha and IL-6 gene transcripts in human keratinocytes. 815 73

The observations of 2 types of CD4+ T cells (Th1 and Th2), which can be distinguished by their different cytokine profiles, has led to the possibility that analysis of cytokine profiles produced locally within transplanted allografts could be predictive of rejection or acceptance of that graft. We have investigated the expression of IL-2 and TNF beta (Th1 type cytokines), IL-4 and IL-10 (Th2 type cytokines), and the proinflammatory cytokines TNF alpha and IL-1 beta in sequential endomyocardial biopsies collected from 12 cardiac transplant recipients during the first 4 months after transplantation, by the analysis of RNA extracted from each biopsy by reverse transcriptase-polymerase chain reaction. The results obtained were compared with histopathological and clinical indicators of rejection. IL-2 was found in all severe (grade 3), in 57% of moderate (grade 2), in 21% of mild (grade 1) rejection, and in only 1 nonrejection (subsequently progressing to grade 3), where rejection was classified by routine histology. IL-4 and IL-10 were absent from grade 3 rejection, but present in 24% (IL-4) and in 17% (IL-10) of mild rejection and in a single nonrejecting biopsy, respectively. IL-4 was found in 2 cases of moderate rejection, and IL-10 in 1 case of moderate rejection. Statistical analysis showed that the presence of IL-2 positively correlated with both mild and moderate rejection, while IL-4 correlated with mild rejection (P < or = 0.05). IL-1 beta, TNF alpha, and TNF beta were found in both rejecting and nonrejecting biopsies, with no significant differences between the histological grades. Our results suggest that in the human situation, IL-2 and IL-4 may indeed be important in the modulation of rejection.
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PMID:Local production of cytokines in the human cardiac allograft. A sequential study. 818 71

In pulmonary sarcoidosis or experimental granuloma formation, interleukin-1 beta (IL-1 beta) or tumor necrosis factor alpha (TNF-alpha) are considered to play important roles during inflammatory evolution. In order to examine whether IL-1 beta or TNF-alpha mRNA expression on lung macrophages relates to the disease activity or clinical course, ten cases with pulmonary sarcoidosis were divided into two groups: five cases who had a disease duration of more than 10 years (14.6 +/- 4.4 years; group A), and 5 cases with duration of less than 3 years (1.7 +/- 1.1 years; group B). All cases showed both abnormal radiographs and elevated serum angiotensin converting enzyme activities. We compared the 10 cases with 12 healthy individuals as normal control (6 nonsmokers: NS and 6 current smokers: S), and 5 cases with idiopathic pulmonary fibrosis (IPF) as disease control. Lavage macrophages were purified by rosette forming method and plastic adhesion was then performed for 1 hour. Thereafter mRNA was extracted by AGPC method and amplified by reverse transcriptase-polymerase chain reaction (RT-PCR) (20 cycles). The results showed that IL-1 beta mRNA was detected in all materials studied, but TNF-alpha mRNA expression was different among the groups: 5/5 (100%) in group A, 1/5 (25%) in group B, 5/5 (100%) in IPF, and 12/12 (100%) in normal controls. The absence of detection of TNF-alpha mRNA (rapid down regulation) in pulmonary sarcoidosis may relate to spontaneous regression, because a substantial number of cases in group B showed spontaneous regression in their natural course.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Differential detection of IL-1 beta and TNF-alpha mRNA on lung macrophages from patients with pulmonary sarcoidosis]. 825 14

Bone marrow (BM) and peripheral blood (PB) cells from patients with juvenile chronic myelogenous leukemia (JCML) exhibit spontaneous in vitro proliferation. Several cytokines including granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-1 beta (IL-1 beta), and tumor necrosis factor alpha (TNF alpha) have been implicated in supporting the growth of leukemic monocyte-macrophage colonies either by autocrine or paracrine pathways. In seven untreated JCML patients, we investigated the role of IL-1 in the spontaneous growth of these cells by specifically blocking IL-1 receptors. The IL-1 receptor antagonist (IL-1 Ra) was added to the clonogenic assays, and in each case significant (mean = 63%, range = 35% to 82%) inhibition of spontaneous proliferation was observed. Uncultured circulating cells from PB or BM of four out of five patients expressed IL-1 beta-specific mRNA and secreted the protein into the culture supernatants. Moreover, by means of reverse transcriptase-polymerase chain reaction (RT-PCR), we demonstrated that most of the spontaneously growing leukemic colony-forming unit cells (CFU-C) obtained from BM cells of two patients were positive for the presence of the IL-1 beta-specific mRNA. Despite the presence of a measurable amount of GM-CSF in JCML cell culture supernatants, GM-CSF-specific mRNA in CFU-C cells of four cases was not detected by RT-PCR. These data further support a central role for IL-1 beta in the pathogenesis of JCML and suggest that the use of IL-1 Ra could represent a novel therapeutic strategy against this disorder.
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PMID:Suppression of juvenile chronic myelogenous leukemia colony growth by interleukin-1 receptor antagonist. 794 96

OL-2, a highly branched (1-->3)-beta-D-glucan, is an antitumor glucan showing strong hematopoietic activity with weaker adjuvant activity than schizophyllan (SPG), also an antitumor glucan and one which is clinically used. This paper deals with the gene expression of the interleukin 1 (IL-1) family in mice by OL-2 and SPG in order to characterize the immunopharmacological activity. Gene expression was examined by reverse transcriptase-polymerase chain reaction method. Intraperitoneal administration of OL-2 (250 micrograms/mouse) expressed all three genes of IL-1 alpha, beta, and IL-1 receptor antagonist (IL-1ra) in the peritoneal exudate cells, while SPG induced a strength of IL-1 alpha mRNA comparable to that by OL-2 but a weaker level of IL-1 beta mRNA. SPG did not induce IL-1ra. Similar patterns were seen in spleen and liver by OL-2 or SPG administration. These findings suggest that the immunopharmacological characteristics of (1-->3)-beta-D-glucan are regulated under the gene expression of the IL-1 family.
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PMID:Expression of interleukin 1 family mRNAs by a highly branched (1-->3)-beta-D-glucan, OL-2. 828 38

Sindbis virus (SV) causes an acute encephalomyelitis in mice. A T cell-dependent inflammatory response is first detected 3 days after infection and includes T cells, B cells, and macrophages. The cytokines produced locally by intrinsic cells of the brain in response to infection and by infiltrating mononuclear cells and their contributions to outcome of infection have not been identified. Semiquantitative reverse transcriptase-PCR was used to evaluate the expression of mRNAs for IL-1 beta, IL-2, IL-4, IL-6, IL-10, TNF-alpha, leukemia inhibitory factor (LIF), and TGF-beta in the brain during fatal and nonfatal SV encephalitis of immunocompetent BALB/cJ and immunodeficient scid/CB17 mice. IL-1 beta and IL-6 mRNAs were detected in uninfected mice before infection and were up-regulated within 24 h. TGF-beta mRNA was also constitutively expressed in uninfected mice. LIF mRNA was occasionally detected in uninfected mice but increased in amounts only in BALB/cJ not scid mice after infection. TNF-alpha, IL-4, and IL-10 mRNAs were not found in uninfected mice but were induced within 24 h and continued to rise through 7 days after infection with substantially higher levels in BALB/cJ than scid mice. These data suggest that intrinsic brain cells produce IL-1, IL-4, IL-6, IL-10, LIF, and TGF-beta mRNAs in response to viral infection. IFN-gamma and IL-2 mRNAs were detected only in BALB/cJ mice and not until 3 days after infection with the initiation of inflammation. IL-4 and IL-10 mRNAs were more persistent and more easily detectable than IL-2 and IFN-gamma mRNAs. These data suggest a predominant type 2 cytokine response in the brain during SV encephalitis. BALB/cJ mice infected with a neurovirulent strain of SV (NSV), had 100% mortality, whereas NSV-infected scid mice developed persistent nonfatal infection. Inflammation was more intense in NSV-infected mice, however, no substantial differences in cytokine mRNA levels were detected when compared with mice with nonfatal SV infection suggesting that the cytokines measured do not in and of themselves lead to fatal central nervous system disease.
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PMID:Intracerebral cytokine mRNA expression during fatal and nonfatal alphavirus encephalitis suggests a predominant type 2 T cell response. 830 Nov 32

Many reports document that bone marrow stromal cells or their cytokine products can influence the formation of B cells in vitro. Most of this data comes from studies using lines or clones of stromal cells after multiple passage in culture, which could alter gene expression. Our aim in the present study was to determine which cytokines are produced by normal stromal cells under conditions that promote B lymphopoiesis. Primary cultured stromal cells were isolated on FACS from active Whitlock cultures. These cells proved to be relatively homogeneous in expression of cell surface antigens (CD44, VCAM-1, MECA10, and a molecule marked by hamster anti-mouse 8.28 monoclonal antibody). RNA from unselected Whitlock cultured adherent cells and sorted stromal cells from the same cultures were subjected to reverse transcriptase polymerase chain reaction to assess constitutive expression of several cytokine genes. Transcripts for interleukin-1 beta (IL-1 beta), IL-7, macrophage (M)-colony-stimulating factor (CSF), stem cell growth factor (SCGF), insulin-like growth factor 1 (IGF-1) and occasionally leukemia inhibitory factor were detected in RNA from intact cultures. Messages for IL-7, M-CSF, and SCGF were selectively contained within the isolated stromal cell fraction; whereas, IL-1 beta was found solely within the non-stromal cell fraction. IGF-1 was transcribed by both stromal cells and macrophages in Whitlock cultures. No evidence was found for constitutive expression of IL-1 alpha, IL-4, IL-6, or granulocyte-macrophage-CSF. This is in contrast to some reported stromal cell lines and clones. To determine if all primary stromal cells from active lymphopoietic cultures produced IL-7, the isolated cells were stained to reveal cytoplasmic IL-7 protein. A majority of the cells produced IL-7, but about 20% had no detectable IL-7 protein. Taken together, our results suggest that the primary stromal cells are a distinguishable cell type but functional subsets may exist. In regard to the differences in IL-7 production, the primary cell phenotype appears to mirror at least one division noted among the stromal cell lines.
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PMID:Cytokine production and heterogeneity of primary stromal cells that support B lymphopoiesis. 834 42

The lymphokine profiles were determined in the skin lesions of the three distinct clinical forms of American cutaneous leishmaniasis (ACL), using a reverse transcriptase polymerase chain reaction (RT-PCR) and primers for various lymphokines. The message for interferon-gamma (IFN-gamma), tumour necrosis factor-beta (TNF-beta), and IL-8 was expressed in the three clinical forms of ACL. IL-1 beta mRNA was expressed in most localized (LCL) and mucocutaneous (MCL) leishmaniasis, but in only few of the diffuse cutaneous leishmaniasis (DCL). IL-2 mRNA was detected in about half of the lesions, with more prominent values for MCL. IL-4 mRNA was present in most lesions from the three clinical forms, but markedly increased in DCL. IL-5 and IL-10 mRNAs were expressed in all MCL and in half of the DCL lesions and weakly expressed in LCL lesions. IL-10 mRNA was more abundant in MCL lesions. In contrast, IL-6 and TNF-alpha mRNAs were expressed in a large number of LCL. In MCL, IL-6 mRNA was expressed in most cases and TNF-alpha mRNA in all the cases. In DCL, IL-6 mRNA was absent and TNF-alpha mRNA was weakly expressed. These results suggest that most T cells present in the MCL and DCL lesions secrete a mixture of type 1 and type 2 cytokine patterns, but in DCL granulomas type 2 cytokines predominate. In LCL the cytokine patterns show a mixture of type 1 and type 0 with a preponderance of IFN-gamma over IL-4, and low levels of IL-5 and IL-10. The lack of IL-6 and TNF-alpha mRNAs, and the low expression of IL-1 beta in DCL lesions suggest a defect in the antigen-processing cells that may account for the state of unresponsiveness in these patients.
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PMID:Determination of the cytokine profile in American cutaneous leishmaniasis using the polymerase chain reaction. 844 70


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