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phytohemagglutinin/necrosis
L'enllaç es desa al porta-retalls
Pàgina 1 des de 593 resultats
The synergistic effect of phytohemagglutinin and interferon-gamma on the expression of tumor necrosis factor-alpha from RAW 264.7 cells.
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Tumor necrosis factor-alpha (TNF-alpha) is a major cytokine of host immune reaction by foreign agents. Phytohemagglutinin (PHA) is a dynamic contributor to mitogenic stimulation and augmentation of host immune defense. Interferon-gamma (IFN-gamma) induces induction of cytokines in macrophages and
Increased production of tumor necrosis factor-alpha and release of soluble CD4 and CD8 molecules, but decreased responsiveness to phytohemagglutinin in patients with nasopharyngeal carcinoma.
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Twelve patients with nasopharyngeal carcinoma (NPC) were studied for spontaneous and phytohemagglutin (PHA)-stimulated production of cytokines, soluble markers and [3H] thymidine incorporation by mononuclear cells. The same number of patients with skin cancer and healthy subjects were used as
[Secretion of interleukin 2, 6 and tumor necrosis factor by peripheral blood mononuclear cells in patients with uveitis induced by phytohemagglutinin or lipopolysaccharide].
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The aim of the study was to determine the concentration of selected cytokines secreted by peripheral blood mononuclear cells (PBMC) of patients with uveitis. We determined the spontaneous secretion and PHA- or LPS-induced production of IL-2, IL-6 and TNF in supernatants. The concentration of
Enhancement of release of granulocyte- and granulocyte-macrophage colony-stimulating factors from phytohemagglutinin-stimulated sorted subsets of human T lymphocytes by recombinant human tumor necrosis factor-alpha. Synergism with recombinant human IFN-gamma.
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The influence of purified recombinant human TNF-alpha (rhuTNF-alpha) was assessed, alone and in combination with purified recombinant human IFN-gamma (rhuIFN-gamma), for its effects on enhancing release from human T lymphocytes of activities that stimulate colony formation by granulocyte-macrophage,
Release kinetics of tumor necrosis factor-α and interleukin-1 receptor antagonist in the equine whole blood.
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BACKGROUND
Horses are much predisposed and susceptible to excessive and acute inflammatory responses that cause the recruitment and stimulation of polymorphnuclear granulocytes (PMN) together with peripheral blood mononuclear cells (PBMC) and the release of cytokines. The aim of the study is to
Both interleukin 1 and tumor necrosis factor enhance thymocyte proliferation.
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One of the biological activities of interleukin 1 (IL1), the lymphocyte-activating function, is usually quantitated by measuring the effect on thymocyte proliferation in the presence of a T cell mitogen. Tumor necrosis factor (TNF) is also produced by activated macrophages, and it has recently been
Natural human IgG inhibits the production of tumor necrosis factor-alpha and interleukin-1 alpha through the Fc portion.
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The overproduction of cytokines such as the tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 alpha (IL-1 alpha) may cause further deterioration in the already critical condition of patients with shock, sepsis, and acute inflammation. The effectiveness of infusion therapy of natural human
Interferon and tumor necrosis factor production by peripheral blood leukocytes of patients with infectious mononucleosis.
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Blood samples from 29 patients with infectious mononucleosis (IM) in phases of acute disease and convalescence were obtained. Interferon alpha (IFN-alpha) and tumor necrosis factor alpha (TNF-alpha) activity was detected in sera of patients both in: acute and convalescence phase, however when IFN
Increase in tumor necrosis factor-alpha mRNA but not perforin mRNA expression in response to two newly characterized anti-LFA-1 monoclonal antibodies.
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We have generated two monoclonal antibodies (mAb), designated anti-1B11 and anti-4F9, directed to the human lymphocyte-function-associated antigen-1 (LFA-1). Indirect immunofluorescence with both mAb showed a bimodal distribution of antigen on the surface of T, natural killer (NK), and
Immunosuppressive effect of infectious pancreatic necrosis virus on rainbow trout (Oncorhynchus mykiss).
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The infectivity of infectious pancreatic necrosis virus (IPNV) for rainbow trout (Oncorhynchus mykiss) mononuclear leukocyte subpopulations was investigated to determine the mechanisms of immunosuppression caused by the virus. IPNV was recovered from nylon wool-adherent, surface immunoglobulin
Tumor necrosis factor in familial Mediterranean fever.
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OBJECTIVE
The pleiotropic inflammatory effects of tumor necrosis factor (TNF) prompted a study of this cytokine in familial Mediterranean fever (FMF), a recurrent polyserositis of unknown etiology.
METHODS
Thirty-six asymptomatic and 24 patients with acute FMF were studied and compared with 20
Single-wall carbon nanotubes (SWCNT) induce cytotoxicity and genotoxicity produced by reactive oxygen species (ROS) generation in phytohemagglutinin (PHA)-stimulated male human peripheral blood lymphocytes.
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Single-wall carbon nanotubes (SWCNT) possess a small size, large surface area, and high reactivity, which enable them to permeate the cytoplasmic or nuclear membrane and attach to biological molecules. During medical applications, SWNCT are usually administered intravenously, which enhances
Production of lymphotoxin and tumor necrosis factor by human neonatal mononuclear cells.
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Lymphotoxin (LT) and tumor necrosis factor (TNF) are cytokines with many common biologic effects including antiviral activity and induction of fever and the acute phase response; despite common effects, they are molecularly distinct. Because neonates are unduly susceptible to viral infection and
Abrogation of in vitro suppression of human immunodeficiency virus type 1 (HIV-1) replication mediated by CD8+ T lymphocytes of asymptomatic HIV-1 carriers by staphylococcal enterotoxin B and phorbol esters through induction of tumor necrosis factor alpha.
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CD8+ T lymphocytes of asymptomatic human immunodeficiency virus type 1 (HIV-1) carriers (AC) suppress HIV-1 replication in vitro. Failure of host defense mechanisms and increased virus proliferation are associated with disease progression. The exact mechanisms inducing these changes at the advanced
Elevated release of tumor necrosis factor-alpha and interferon-gamma by bronchoalveolar leukocytes from patients with bronchial asthma.
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Bronchoalveolar lavage (BAL) leukocyte-secreted cytokines are considered to be important mediators of the inflammatory and allergic reactions in the lung. This study examines quantitative changes in the level of tumor necrosis factor-alpha (TNF alpha) and interferon-gamma (IFN gamma) production in
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