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Antibody-dependent cell cytotoxicity ADCC

NE NK activity Antibody-Dependent Cell Cytotoxicity (ADCC) Decrease Decrease... [Pg.531]

Halothane-induced hepatitis seems to be mediated by both humoral and cell-mediated aspects of the immune system. Thus, both specific circulating antibodies and cytotoxic T lymphocytes are involved. One suggestion is that the mechanism involves antibody-dependent cell cytotoxicity (ADCC). [Pg.375]

An alternative mechanism is based on non-complement dependent cytotoxicity, e.g., food allergen stimulation of mechanisms of antibody dependent cellular cytotoxicity (ADCC), cytotoxicity of natural killer cells or macrophages. The contribution of ADCC in gastroenteropathy of children induced by cow s milk allergens was demonstrated by Owen et al. (1993). [Pg.120]

ADCC antibody-dependent cell cytotoxicity, adenocarcinoma malignant epithelial tumor, adenoma benign epithelial tumor of glandular origin. [Pg.409]

Figure 22.2 Cellular activation by CpG DNA. CpG DNA directly activates dendritic cells (DCs), monocytes and macrophages, to express increased levels of co-stimu-latory molecules, to increase antigen presentation, and to secrete high levels of chemokines and cytokines, such as interleukin 12 (IL-12), interferon-a(IFN-a), and tumor necrosis factor-a (TNF-a), and monocytes and macro-phages have increased antibody-dependent cellular cytotoxicity (ADCC) activity. NK cells are induced to express IFN-7 by these cytokines acting in concert with CpG, and have increased lytic activity. B cells rapidly produce IL-b and IL-10 and express increased levels of costimulatory molecules. B cells rapidly enter the cell cycle and become resistant to some forms of activation-induced cell death. T cells are not directly activated by CpG, but because of the T helper 1 (Thl)-like cytokine environment, and the increased antigen presenting cell (APC) activity, antigen-specific Thl cells and cytotoxic T lymphocytes (CTL) are generated. Figure 22.2 Cellular activation by CpG DNA. CpG DNA directly activates dendritic cells (DCs), monocytes and macrophages, to express increased levels of co-stimu-latory molecules, to increase antigen presentation, and to secrete high levels of chemokines and cytokines, such as interleukin 12 (IL-12), interferon-a(IFN-a), and tumor necrosis factor-a (TNF-a), and monocytes and macro-phages have increased antibody-dependent cellular cytotoxicity (ADCC) activity. NK cells are induced to express IFN-7 by these cytokines acting in concert with CpG, and have increased lytic activity. B cells rapidly produce IL-b and IL-10 and express increased levels of costimulatory molecules. B cells rapidly enter the cell cycle and become resistant to some forms of activation-induced cell death. T cells are not directly activated by CpG, but because of the T helper 1 (Thl)-like cytokine environment, and the increased antigen presenting cell (APC) activity, antigen-specific Thl cells and cytotoxic T lymphocytes (CTL) are generated.
Type II Drugs often modify host proteins, thereby eliciting antibody responses to the modified protein. These allergic responses involve IgG or IgM in which the antibody becomes fixed to a host cell, which is then subject to complement-dependent lysis or to antibody-dependent cellular cytotoxicity (ADCC). [Pg.1356]

MoAb, Pa no rex) Signal Pathway Inhibitors tumor-specific glycoprotein located on colorectal tumor cells antitumor activity via antibody-dependent cellular cytotoxicity (ADCC) vomiting, infusion-related reactions (fever, chills) ... [Pg.2401]

Trastazumab is a monoclonal antibody. It is a recombinant DNA-derived humanized monoclonal antibody that selectively binds with high afhnity to the extracellular domain of the HER2. It inhibits the proliferation of human tumor cells that over express HER2 and mediates antibody-dependent cellular cytotoxicity (ADCC). It is indicated in breast cancer. [Pg.701]

The anti-CD20 Mab had been purposely engineered with human constant regions (IgGl kappa isotype) to ensure that it would effectively bind complement and, through Fc receptors, effector cells so that it could effect complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) [5, 6] (Fig. 1). This was confirmed in vitro. Additionally, in vivo experiments in monkeys revealed immediate, profound, and specific B-cell depletion with recovery within 100 days. The effects of the antibody on the human immune system were unknown. It was expected to produce B-cell depletion and... [Pg.214]


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See also in sourсe #XX -- [ Pg.130 ]

See also in sourсe #XX -- [ Pg.54 , Pg.323 , Pg.325 , Pg.329 , Pg.344 , Pg.345 ]




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