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Cells macrophage

The first equation states that cytotoxic cells grow only if helper cells, macrophages and the virus are all present. The second equation implies that, when the virus is not present, helper cells grow if macrophages and/or helper cells are present. The third equation implies that macrophages grow both when the virus is present and there is already a concentration of macrophages. The last equation describes the... [Pg.428]

Expression (Mouse) Tissues lungs, Cells myeloid leukocytes, neutrophils, T-cells, macrophages, mast cells, eosinophils Tissues lung, skin, small intestine Cells macrophages, fibroblasts, leukocytes Tissues lung, skin, brain, small intestine, spleen Cells macrophages, fibroblasts, endothelial cells, leukocytes... [Pg.688]

Non-neuronal cells (including astrocytes, mechan-osensory hair cells, macrophages, keratinocytes, endothelial cells of the vascular system, muscle cells, lymphocytes, intestinal epithelial cells and various cell-types of the lungs)... [Pg.852]

NF-kB regulates both innate and adaptive immune responses ( immune defense) [2]. Understanding the function of NF-kB in the development, maintenance, and activation of cells from the immune system (including hematopoietic cells, macrophages, dendritic cells, B and T lymphocytes) has greatly benefited from the analysis of knockout mice in which individual NF-kB family members were defective. [Pg.886]

Class 2 MHC molecules are expressed on the surface of B cells, macrophages, monocytes, various antigen-presenting cells (APCs) and certain cells of the T-cell famify. [Pg.294]

From endothelial cells macrophages/monocytes smooth muscle ceils... [Pg.45]

Inflammatory cell phenomenon are also contributors to lipid peroxidation. Activated neutrophils may adhere to damaged endothelium and amplify traumatic, ischaemic or ischaemia-reperfiision injury. Many cyclooxygenase products of the metabolism of atachidonic acid modulate the inflammatory responses of cells. Macrophages, neutrophils and microglia are important sources of reactive oxygen at the injury site. When activated, they produce a respiratory burst that is traced to activated nicotinamide adenine dinucleotide (NADPH/NADH) oxidase. [Pg.273]

Dysfunction of the endothelium allows lipoproteins, predominantly low-density lipoprotein (LDL) cholesterol, and inflammatory cells, namely monocytes and T lymphocytes, to migrate from the plasma to the sub-endothelial space. Monocyte-derived macrophages ingest lipoproteins to form foam cells. Macrophages also secrete growth factors that promote smooth muscle cell migration from the media to the intima. A fatty streak consists of lipid-laden macrophages and smooth muscle cells and is the earliest type of atherosclerotic lesion. [Pg.66]

An APC is a cell that displays a foreign antigen complex with MHC on its cell surface. Its major responsibility is to present these foreign antigens to T cells. T cells can identify this complex using their T-cell receptors (TCRs). There are three main types of APCs dendritic cells, macrophages, and activated B cells. Dendritic cells (DCs) are present in tissues that... [Pg.833]

Yang X, Lu P, Ishida Y, Kuziel WA, Fujii C, Mukaida N. Attenuated liver tumor formation in the absence of CCR2 with a concomitant reduction in the accumulation of hepatic stellate cells, macrophages and neovascularization. Int J Cancer 2006 118 335-345. [Pg.350]

Main producer cells Bone marrow stromal cell Macrophages Fibroblasts Lymphocytes Myoblasts Osteoblasts Monocytes Fibroblasts Endothelial cells Macrophages T-lymphocytes Fibroblasts Endothelial cells... [Pg.269]

Main target cells Neutrophils. Also other haemopoietic progenitors and endothelial cells Macrophages and their precursor cells Haematopoietic progenitor cells Granulocytes Monocytes Endothelial cells Megakaryocytes T-lymphocytes Erythroid cells... [Pg.269]

Cyclosporine reduces production of cytokines involved in T-cell activation and has direct effects on B cells, macrophages, bone, and cartilage cells. Its onset appears to be 1 to 3 months. Important toxicities at doses of 1 to 10 mg/kg/day include hypertension, hyperglycemia, nephrotoxicity, tremor, GI intolerance, hirsutism, and gingival hyperplasia. Cyclosporine should be reserved for patients refractory to or intolerant of other DMARDs. It should be avoided in patients with current or past malignancy, uncontrolled hypertension, renal dysfunction, immunodeficiency, low white blood cell or platelet counts, or elevated Ever function tests. [Pg.52]

It is reasonable to presume that the immunogenic and adjuvant activity of lipospheres may be the result of a combination of factors. These factors may include a focused and enhanced delivery of the antigen to an antigen-presenting cell (macrophage) and protection of the antigen from metabolic destruction at other sites in the body that do no participate in the immune response. [Pg.11]

Follow-on studies are also recommended as needed. These include determination of potential test article effects on blood or tissue immunophenotypes (by flow cytometry or immunohistochemistry), natural killer cell, macrophage, or neutrophil function, host resistance to infection or tumors, and cell-mediated immunity. The important issue in all of these guidelines is this do not ignore signs of immunotoxicity, and assess these findings when observed. [Pg.30]

Schmitt, D. A. and Ullrich, S. E., Exposure to ultraviolet radiation causes dendritic cells/ macrophages to secrete immune suppressive IL-12p40 homodimers, J. Immunol. 165, 3162-3167, 2000. [Pg.274]

The effect of MAPK activation on cellular processes that affect cell function and the resulting pharmacology has been delineated using modem techniques such as knock-out cells and animals [1,3,6]. Activation of MAPK in inflammatory cells such as T-cells, B-cells, macrophages and eosinophils leads to expression and/or activation of pro-inflammatory genes and mediators such as interleukin-1(3 (IL-1(3), TNFa, IL-6, chemokines [e.g., IL-8, macrophage inflammatory factor-1 a, (3 (MIP-la,[3)J, MMPs and toxic molecules such as free radicals and nitric oxide [1,3]. These pro-inflammatory mediators induce cellular proliferation, differentiation, survival, apoptosis and tissue degradation/destruction and help induce chronic inflammation. Inhibition of any one or more of the MAPK family... [Pg.267]

DCCD and vanadate. This indicates an active process energised by ATP. Ferrozine inhibition of Fe2+ and Fe3+ uptake implied the concerted involvement of both a Fe3+ reductase and FeoB in the uptake of iron supplied as Fe3+. It is concluded that FeoB-mediated Fe2+ represents a major pathway for H. pylori iron sequestration [189], In addition, growth experiments on the human pathogen L. pneumophila using artificial media, as well as replication studies within iron-depleted Hartmannella vermiformis amoebae and human U937 cell macrophages, provided evidence that the FeoB transporter is important for extracellular growth and intracellular infectivity [190],... [Pg.310]

Includes lymphokines, monokines, and cytokines produced by T cells, macrophages, and other cells, respectively. Source Extracted and modified from Golub and Green, 1991. [Pg.541]

Since cellular immunity results in the release of chemotactic lymphocytes that in turn enhance phagocytosis, a deficiency in cellular immunity may also result in chronic infections. Cellular immunity is mediated by T cells, macrophages, and NK cells involved in complex compensatory networks and secondary changes. Immunosuppressive agents may act directly by lethality to T cells, or indirectly by blocking mitosis, lymphokine synthesis, lymphokine release, or membrane receptors to lymphokines. In addition, cellular immunity is involved in the production and release of interferon, a lymphokine that ultimately results in blockage of viral replication (Table 15.4). Viruses are particularly susceptible to cytolysis by T cells since they often attach to the surface of infected cells. Thus, immunosuppression of any of the components of cellular immunity may result in an increase in protozoan, fungal, and viral infections as well as opportunistic bacterial infections. [Pg.543]

As described previously, the humoral immune response results in the proliferation, activation, and subsequent production of antibodies by B cells following antigenic exposure and stimulation. The functionality and interplay between the three primary types of immune cells (macrophage, B cells, and T cells) required to elicit a humoral response can be assessed through various in vitro assays using cells from the peripheral blood or lymphoid tissues. [Pg.564]


See other pages where Cells macrophage is mentioned: [Pg.429]    [Pg.224]    [Pg.239]    [Pg.541]    [Pg.1081]    [Pg.157]    [Pg.122]    [Pg.124]    [Pg.210]    [Pg.286]    [Pg.8]    [Pg.234]    [Pg.433]    [Pg.829]    [Pg.9]    [Pg.160]    [Pg.179]    [Pg.210]    [Pg.307]    [Pg.189]    [Pg.356]    [Pg.205]    [Pg.135]    [Pg.153]    [Pg.309]    [Pg.380]    [Pg.382]    [Pg.384]    [Pg.385]    [Pg.552]   
See also in sourсe #XX -- [ Pg.155 ]




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Antigen-presenting cell interactions macrophages

Antigen-presenting cells macrophages

Cell lines monocytes/macrophages

Cell, animal macrophage

Cell-mediated immunity macrophage activation

Granulocyte/macrophage colony-stimulating mast cells

IL-2 production by macrophages/dendritic cell

Immune cells, macrophages

Intracellular macrophage cell

Macrophage cell culture

Macrophage cell line

Macrophage cell line inflammatory protein

Macrophage cell surface antigen

Macrophage-T cell interactions

Macrophage-dendritic cell interaction

Macrophage-dendritic cell regulation

Macrophage-derived foam cells

Macrophages and T helper cells

Macrophages foam cells

Macrophages malignant cells

Mouse monocyte/macrophage cell line

Murine monocyte/macrophage cell line

Nitric oxide cells/macrophages

RAW 264-7 macrophage cell lines

Target Cells for Macrophage Stimulating Protein

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