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Macrophage-T cell interactions

Through regulation of gene transcription, cyclosporine inhibits interleukin-1 and interleukin-2 receptor production and secondarily inhibits macrophage-T-cell interaction and T-cell responsiveness (see Chapter 55). T-cell-dependent -cell function is also affected. [Pg.807]

Hume CSF-1 itself causes total immune suppression if you administer it to a mouse, but it is also made as an integral membrane protein. It would actually lead to macrophage T cell interactions that would not normally happen. This could be a signalling pathway to polarization. [Pg.101]

Evidence for the participation of histocompatibility gene products in macrophage—T cell interactions... [Pg.153]

The evidence to date indicates that the cell-interaction genes involved in T-B cell interactions map in the / region, more specifically in the I-A and/or I-B subregions. The location of Cl genes involved in macrophage-T cell interactions and those possibly involved in T-T interactions are not as clearly mapped as yet. [Pg.157]

Agostini C, Trentin L, Perin A, et al. Regulation of alveolar macrophage-T cell interactions during Thl-type sarcoid inflammatory process. Am J Physiol 1999 277(2 pt 1) L240-L250. [Pg.181]

Complications of atherosclerosis are the leading cause of morbidity and mortahty in developed countries. It can be considered as a chronic inflammation resulting from interaction between modified lipoproteins, monocyte-derived macrophages, T cells, and the normal cellular elements of the arterial wall [107-109]. The earliest lesion is a pure inflammatory lesion consisting of monocyte-derived macrophages and T cells. The presence of monocytes in every phase of atherosclerosis, and of hydrolytic enzymes secreted by these and other cells, play a central role in different stages of the disease, particularly in the resorption of the fibrous cap leading to plaque rupture. [Pg.1281]

FIGURE 53-2 Cytokine cell interactions. Macrophages, T cells, B cells, and marrow stem cells interact via several cytokines (IL-1, IL-2, IL-3, IL-4, IFN [interferon]-"X GM-CSF, and G-CSF) in response to a bacterial or a foreign antigen challenge. [Pg.932]

A recent example of a CA model of the immune response in AIDS is Pandley s four-cell model using interactions among macrophages (= M) containing parts of the virus on their surface, helper T cells (= H), cytotoxic T cells (= C) and the virus (= V) ([pand89], [pandQl]) ... [Pg.428]

A large number of cells are involved in the immune response and all are derived fiom the multipotential stem cells of the bone marrow. The predominant cell is the lymphocyte but monocytes-macrophages, endothelial cells, eosinophils and mast cells are also involved with certain immune responses. The two types of immunity (humoral and cell-mediated) are dependent on two distinct populations of lymphocytes, the B cells and the T cells respectively. Both the humoral and the cell-mediated systems interact to achieve an effective immune response. [Pg.285]

Figure 9.3 Activation of T-cells by interaction with macrophage-displayed antigen. Activation results in IL-2 production, which acts in an autocrine manner to stimulate further T-cell growth and division. IL-2 thus represents the major regulatory molecule responsible for stimulation of cell-mediated immunity. Note that it was initially believed that binding of presented antigen alone was insufficient to trigger T-cell activation. It was thought that co-stimulation with IL-1 was reguired. However, the assay used to detect the co-stimulation was found not to be specific for IL-1 alone. The role of IL-1 as a co-stimulator of T-cell activation is now believed to be minimal at most... Figure 9.3 Activation of T-cells by interaction with macrophage-displayed antigen. Activation results in IL-2 production, which acts in an autocrine manner to stimulate further T-cell growth and division. IL-2 thus represents the major regulatory molecule responsible for stimulation of cell-mediated immunity. Note that it was initially believed that binding of presented antigen alone was insufficient to trigger T-cell activation. It was thought that co-stimulation with IL-1 was reguired. However, the assay used to detect the co-stimulation was found not to be specific for IL-1 alone. The role of IL-1 as a co-stimulator of T-cell activation is now believed to be minimal at most...

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See also in sourсe #XX -- [ Pg.172 ]




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