Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To identify viral antigens, the types of infiltrating mononuclear cells and cytokine bearing cells, the frozen brain tissue sections form a patient with herpes simplex encephalitis who died on 12th hospital days, were examined by immunocytochemistry methods and combined immunocytochemistry and in situ hybridization. The avidin-biotin peroxidase complex (ABC) techniques were applied for the detection of antigens. All monoclonal antibodies to Leu series and polyclonal antisera to lymphotoxin (LT), interleukin-6 (IL-6) and interferon-gamma (IFN-gamma) were purchased form Becton Dickinson Co., and Genzyme Co., (USA) respectively. A large number of neurons and glial cells staining positively HSV-1 antigens were found in the gray matter. Moreover, although a moderate number of HLA-DR (Ia) positive cells were found in the parenchyma, there were few cells displaying positively for Leu-3a, Leu-2a and Leu-7 respectively. To evaluate the number of positive cells appeared in the brain tissues, Leu stain for 4, 2a, 3a, 7, 12 and HLA-DR demonstrated 1.6%, 0.4%, 0.9%, 0.7% and 10% respectively. In addition, numerous number of IFN-gamma positive cells were detected around the lesion and randomly distributed thoroughly the lesion. IL-6 positive cells and LT positive cells were also similar in distribution to IFN-gamma positive cells. Moreover, in simultaneous detection of HLA-DR and HSV-1 mRNA by the combined immunocytochemistry and in situ hybridization, there were seen glial cells staining positively for HLA-DR (Ia) and several cells with mRNA.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[The detection and quantitative analysis of viral antigens, infiltrating mononuclear cells, IFN-gamma, LT and IL-6 bearing cells in the frozen brain tissue sections from a patient with herpes simplex encephalitis by immunocytochemistry]. 216 12

The study of monocyte/macrophage functions after human immunodeficiency virus type 1 (HIV-1) infection may help in understanding the pathogenesis of AIDS. The production of four cytokines, tumor necrosis factor alpha (TNF alpha), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and granulocyte-macrophage colony-stimulating factor (GM-CSF), by peripheral blood monocytes/macrophages was evaluated after in vitro infection with HIV-1. HIV-1 infection of these monocytes/macrophages did not result in release of any of these cytokines. Similarly, treatment of uninfected cells with purified recombinant HIV-1 envelope protein did not result in cytokine production. After stimulation with endotoxin or endotoxin plus interferon-gamma, HIV-1-infected monocytes/macrophages produced amounts of TNF alpha, IL-6, GM-CSF, and IL-1 beta comparable to that of uninfected cells. HIV-1 infection does not appear to induce or alter cytokine production by mononuclear phagocytes, which retain the capacity to produce these cytokines after endotoxin stimulation.
 ...
PMID:Production of cytokines by peripheral blood monocytes/macrophages infected with human immunodeficiency virus type 1 (HIV-1). 218 29

Tissue macrophages of the liver (Kupffer cells) release interleukin-6 (IL-6) in vitro. Since Kupffer cells reside in close proximity to hepatocytes, which are major target cells of IL-6, the regulation of IL-6 release by hepatic macrophages has been investigated in this study. Using the hybridoma growth test to detect IL-6, we found that Kupffer cells already maximally release IL-6 at endotoxin concentrations as low as 1.0 ng/ml. The stimulated secretion of IL-6 was increased 4-8-fold by endotoxin when compared to the control macrophages incubated in serum-containing medium alone. The preincubation of macrophages with interferon-gamma enhanced the capacity of Kupffer cells to respond to endotoxin. The secretion of IL-6 could also be induced by interleukin (IL)-1 beta and tumor necrosis factor (TNF-alpha). The most potent inducers, however, were the paramyxoviruses Newcastle Disease Virus and Sendai Virus. The release of IL-6 by macrophages upon stimulation with endotoxin was almost completely inhibited by 1 microM dexamethasone. Whereas 100 nM of prostaglandin E2 (PGE2) inhibited the release of TNF-alpha in rat Kupffer cells, it did not affect the secretion of IL-6.
 ...
PMID:Interleukin-6 release by rat liver macrophages. 229 28

In order to determine if mononuclear cells may be secreting factors capable of modulating fibroblast growth, the in vitro proliferative response of fibroblasts to cytokines known to be secreted by mononuclear cells was measured, using both growth arrested and proliferating cells. Of the cytokines tested, which included interleukin-1 (IL-1), interleukin-2 (IL-2), interleukin-3 (IL-3), interleukin-4 (IL-4), interleukin-6 (IL-6), interferon-alpha (IFN-alpha), interferon-gamma (IFN-gamma), transforming growth factor-alpha (TGF-alpha), transforming growth factor-beta (TGF-beta), platelet derived growth factor (PDGF), and tumor necrosis factor-alpha (TNF-alpha), only TNF-alpha and PDGF had demonstrable growth factor activity. Neither IL-1 alpha nor beta showed any true growth factor activity but were able to enhance the replication of already proliferating cells. No inhibition of proliferation was noted by any of the cytokines with the exception of TNF-alpha and TGF-beta. TNF-alpha in doses greater than 500 ng/ml caused fibroblast death, probably by a prostaglandin related mechanism as fibroblasts remained viable, although non proliferative, when assayed in the presence of indomethacin, a known inhibitor of prostaglandin E2 (PGE2) synthesis. TGF-beta was inhibitory to proliferation at doses greater than 100 ng/ml, while fibroblasts remained viable. This effect was not influenced by indomethacin and hence is unlikely to be PGE2 related.
 ...
PMID:Interaction of immune and connective tissue cells: I. The effect of lymphokines and monokines on fibroblast growth. 231 5

The proliferation and differentiation of astrocytes are fundamental events in the normal development and function of the central nervous system (CNS), and may also contribute to the pathogenesis of a number of neurological diseases. Products of T lymphocytes can stimulate proliferation of astrocytes, but the nature of the T lymphocyte-derived molecule(s) responsible for this response is unknown. The present study was undertaken to examine several well-characterized T lymphocyte-derived factors for their ability to stimulate cultured primary rat astrocytes. While recombinant human interleukin-2 (IL-2), interleukin-3 (IL-3), interleukin-4 (IL-4), interleukin-5 (IL-5), interleukin-6 (IL-6), and rat or human recombinant interferon-gamma (IFN-gamma) have no proliferative effect on astrocytes, a human T cell-derived B cell growth factor (BCGF) does. This BCGF, termed 2B11, had previously been characterized by its ability to enhance the proliferation of anti-mu-stimulated human B cells, while not influencing B cell immunoglobulin synthesis. High performance liquid chromatography (HPLC)-purified 2B11-BCGF (MW approximately 20,000 daltons) stimulates the proliferation of astrocytes in a dose-dependent fashion. Purified 2B11-BCGF also induced morphological differentiation and increased mRNA transcripts for glial fibrillary acidic protein (GFAP) in rat astrocytes. In addition to demonstrating the absence of effect of other known lymphokines, the effect on astrocytes attributed to 2B11-BCGF was confirmed by blocking its activity with a monoclonal antibody specific for 2B11-BCGF. Absorption experiments demonstrated that when BCGF activity was absorbed out by large, activated human B cells, astrocyte-stimulatory activity was also depleted. Rat astrocytes were able to partially absorb out both BCGF and astrocyte-stimulatory activity. These results suggest that 2B11-BCGF is responsible for stimulating astrocyte proliferation, and that human B cells and rat astrocytes may share a similar receptor for BCGF. These findings indicate that the growth and differentiation of astrocytes can be influenced by a T cell-derived lymphokine, 2B11-BCGF, whose activity thus far appears to be distinct from other reported cytokines.
 ...
PMID:Human B cell growth factor enhances proliferation and glial fibrillary acidic protein gene expression in rat astrocytes. 248 87

The suppression of B lymphopoiesis is a major feature of multiple myeloma (MM). In this disease, there is a striking defect in the response of peripheral blood B cells to pokeweed mitogen (PWM). Normally, B-cell activation depends on B-cell growth factors (BCGFs) and B-cell differentiation factors (BCDFs), produced by peripheral blood mononuclear cells. We therefore evaluated whether the production of these cytokines was defective in patients with MM. We have studied the production of BCGFs (using the anti-mu assay) and, particularly, interleukin-2 and interferon-gamma, two well-documented BCGFs. No defect in the production of BCGFs, interleukin-2, and interferon-gamma was found in patients with active (N = 14) or stable (N = 10) MM, compared with healthy donors (N = 13). The production of BCDFs (i.e., overall activity) was also evaluated and, more particularly, that of interleukin-6 (IL-6). This cytokine is a potent BCDF which is essential in the PWM-induced activation of B cells, acting at the terminal stages of B-cell differentiation. Again, no defect in the production of BCDFs and IL-6 was found in patients with MM. Therefore, the ability to secrete cytokines controlling the process of B-cell activation is not affected in such patients. This indicates that the profound failure of humoral immune response is not due to deficiency of peripheral blood mononuclear cells producing these factors.
 ...
PMID:The defect in peripheral blood B-cell activation in patients with multiple myeloma is not due to a deficiency in the production of B-cell growth and differentiation factors. 249 99

Tumor necrosis factor (TNF) and interleukin-1 (IL-1) are cytotoxic for certain tumor cells but have a proliferative effect on normal cells. Here we show that interferon-gamma (IFN-gamma) can be cytotoxic for normal cells, in particular mouse embryonic fibroblasts. The cytotoxicity effect is observed with immuno-purified recombinant mouse IFN-gamma (MuIFN-gamma) at concentrations of 1,000 I.U./ml and can be neutralized by anti-MuIFN-gamma monoclonal antibodies. The effect appears 48 h after initial contact with IFN-gamma and is not influenced by infection of the target cells with mengovirus. Although TNF and IL-1 are not toxic for mouse fibroblasts, they can strongly enhance the IFN-gamma-induced cytotoxicity. Interferon-alpha (IFN-alpha), interferon-beta (IFN-beta) and interleukin-6 (IL-6) neither are cytotoxic themselves nor have any influence on the IFN-gamma-induced cytotoxicity. The cytotoxicity of IFN-gamma, in contrast to that of TNF is inhibited by actinomycin or cycloheximide. These data suggest that the cytotoxic effect of IFN-gamma requires active cooperation of target cells and that the mechanism of action is different from that of the TNF-induced cytotoxicity.
 ...
PMID:Interferon-gamma is cytotoxic for normal mouse fibroblasts: enhancement by tumor necrosis factor and interleukin 1. 249 77

Interleukin-2 (IL-2) plays an essential role in the clonal expansion of antigen-activated T lymphocytes (T cells). In fact, the expression of both IL-2 and IL-2 receptor (IL-2R, p55, CD25) genes is transiently induced upon T cell activation through the interaction of antigen/major histocompatibility complex (MHC) and T cell receptor complex. To elucidate the mechanism(s) of the induced gene expression for IL-2 and IL-2R, we have investigated for the presence of potential transcription factors that specifically interact with regulatory cis-elements. Here, we demonstrate that one such factor mediates the induced expression of both genes. Interestingly, the recognition sequences by this factor are significantly diverse in these two genes and are related to those of immunoglobulin (Ig) kappa chain and MHC class I genes. We provide evidence that this factor indeed binds to the IL-2, IL-2R, and Ig sequence elements with different affinities, thereby affecting the magnitude of gene expression. Interestingly, this factor also binds to other cytokine genes, such as interleukin-6 (IL-6), interferon-gamma (IFN-gamma), and HIV-1 and HTLV-1 LTR sequences.
 ...
PMID:Involvement of a common transcription factor in the regulated expression of IL-2 and IL-2 receptor genes. 251 55

The induction of cytotoxic T lymphocytes (CTL) from CTL precursors requires a combination of antigen and lymphokine signals. To investigate lymphokine requirements for CTL generation, we used an assay in which helper T cell and accessory cell-depleted spleen cells or whole thymocytes were cultured with lectin (Con A) and lymphokines. This culture was followed by assessment of lectin-dependent cytolysis. High concentrations of recombinant interleukin 2 (R-IL 2) (100 U/ml) alone were not sufficient for lectin-mediated CTL induction from thymocytes, whereas 20 to 100 U/ml of R-IL 2 alone could induce a significant lectin-mediated CTL response from accessory cell-depleted spleen cells. Using thymocytes as responders, we found purified or recombinant interferon-gamma (IFN-gamma) did not cause cytolytic activity either in the absence of or in the presence of R-IL 2. However, supernatant from Con A-stimulated rat spleen cells (rat Con A SN) in combination with R-IL 2 could induce cytolytic activity, suggesting that several factors are required for CTL induction. Con A SN was fractionated by gel filtration and the fractions were tested for ability to induce CTL. In the presence of a low level of R-IL 2 (5 U/ml), fractions with a Mr of approximately 31,000 could induce CTL, and this activity was referred to as CTL differentiation factor (CDF). The peak fractions containing CDF activity did not have detectable IL 1, IL 2, IFN-gamma, or CSF activity. However, by add-back experiments and the use of blocking antibodies, a monoclonal antibody against the IL 2 receptor or antibodies against murine IFN-gamma, we demonstrated that CTL induction from mature thymocytes (L3T4-, Lyt-2+) requires CDF activity in addition to IL 2 and IFN-gamma.
 ...
PMID:Requirement for three distinct lymphokines for the induction of cytotoxic T lymphocytes from thymocytes. 309 23

In this report we have extended our previous studies on interleukin 4 (IL-4) [previously termed B-cell stimulatory factor-1 (BSF-1)]. Our results demonstrate that 8 hr of exposure to IL-4 is sufficient to induce maximal expression of Ia antigens. This increase in expression of Ia antigens on resting B cells is due to the direct action of IL-4 on the B cells since adding or removing adherent cells or utilizing low density cultures of B cells at 50-100/culture had no effect on the IL-4-mediated increase in Ia. Monoclonal anti-IL-4 antibody completely abrogated the Ia-inducing activity of IL-4. A variety of other purified lymphokines including interleukin 2 (IL-2), interleukin 1 (IL-1), and a source of either B-cell differentiation factor for IgM (BCDF mu), or B-cell growth factor II (BCGF II), did not alter the expression of Ia antigens on resting B cells. However, interferon-gamma can partially inhibit the IL-4-mediated induction of Ia.
 ...
PMID:The effects of cytokines and adherent cells on the interleukin 4-mediated induction of Ia antigens on resting B cells. 310 99


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>