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Chemokines cytokines

Randolph GJ. Dendritic cell migration to lymph nodes cytokines, chemokines, and lipid mediators. Semin Immunol 2001 13(5) 267-274. [Pg.100]

Broxmeyer HE, Sherry B, Cooper S, et al. Comparative analysis of the human macrophage inflammatory protein family of cytokines (chemokines) on proliferation of human myeloid progenitor cells. Interacting effects involving suppression, synergistic suppression, and blocking of suppression. J Immunol 1993 150(8 Pt... [Pg.132]

Fig. 11.1. Atherogenesis is a persistent inflammatory response that occurs in response to conditions that cause endothelial damage (e.g., hypercholesterolemia and oxLDL). After endothelial cells are activated, they elaborate cytokines, chemokines, and other mediators that recruit mononuclear cells (monocytes and T lymphocytes) to extravasate into the vessel wall where they are activated and release additional proinflammatory factors. Macrophages are able to take up oxLDL via scavenger receptors causing them to differentiate into foam cells and form a fatty streak that progresses to an atheroma with a necrotic lipid core and a fibrous cap. Chemokines can lead to weakening of the fibrous cap and eventual plaque rupture leading to thrombosis and occlusion of the involved vessel. Fig. 11.1. Atherogenesis is a persistent inflammatory response that occurs in response to conditions that cause endothelial damage (e.g., hypercholesterolemia and oxLDL). After endothelial cells are activated, they elaborate cytokines, chemokines, and other mediators that recruit mononuclear cells (monocytes and T lymphocytes) to extravasate into the vessel wall where they are activated and release additional proinflammatory factors. Macrophages are able to take up oxLDL via scavenger receptors causing them to differentiate into foam cells and form a fatty streak that progresses to an atheroma with a necrotic lipid core and a fibrous cap. Chemokines can lead to weakening of the fibrous cap and eventual plaque rupture leading to thrombosis and occlusion of the involved vessel.
Homo sapiens (compared to Drosophila melanogaster) Large-scale gene duplications with substantial expansion of genes involved in acquired immune response (B cells, T cells, major histocompatibility complex genes, cytokines, chemokines and their receptors), plasma proteases (complement and hemostatic proteins), proteins associated with apoptotic regulation and proteins related to neuronal network formation and electrical coupling... [Pg.18]

Inflammation is the normal host response to infection or injury that mediates immune elimination of pathogens and tissue repair. Inflammatory processes include increased production of cytokines, chemokines, nitric oxide, and eicosanoids by the innate immune system in conjunction with altered leukocyte homing, all of which greatly impact acquired immunity. Aberrant inflammatory responses evoke both acute injury such... [Pg.291]

At least some of the cannabinoid-induced modulation of immune cells, and effects on host resistance to infection, are mediated directly by binding of cannabinoids to CBRs, particularly CBR2. Host immunity to microbes, however, involves many cell types, both immune and non-immune, as well as soluble factors including cytokines, chemokines, neurocytokines, and hormones related to the HP axis. It is therefore likely that a variety of cellular and molecular mechanisms whereby cannabinoids, including THC, affect immune function. [Pg.530]

CC Chemokine Receptor 2 (CCR2) is a member of the G protein-coupled receptor (GPCR) superfamily that serves as the receptor for monocyte chemoattractant proteins 1-4 (MCP-1 to -4), a group of pro-inflammatory chemotactic cytokines (chemokines). CCR2 is the primary chemokine receptor on inflammatory monocytes, and is also expressed on T-cells, dendritic cells, and endothelial cells. Upon ligand engagement, CCR2 mediates both cellular movement and activation. [Pg.211]

Depleting CD4+CD25+ Treg from peripheral blood of non-atopic individuals induces a similar pattern of proliferation and Th2-cytokine production to atopic patients in response to allergen stimulation [16]. CD4+CD25 8h Treg frequency and suppressive activity (both proliferation and cytokine/chemokine production) are reduced... [Pg.152]

CRAMP Murine Immature neutrophils, spleen, respiratory and intestinal epithelia, keratinocytes, testis Cell proliferation/differentiation chemotaxis antiendotoxic adaptive immune polarization in vivo protection cytokine/chemokine induction FPRL1, murine FPRL2... [Pg.194]

The most important clinical application of glucocorticoids and their semisynthetic analogs is their anti-inflammatory activity, discovered in 1949 by Hench and co-workers. The profound anti-inflammatory effects of glucocorticoids arise from the combined effects of these steroids on both the cellular and molecular mediators of inflammation these effects are separate from the metabolic effects described above and further indication of the widespread diversity of macromolecules to which steroids can bind. Glucocorticoids suppress inflammation at the cellular level by downregulating the concentration, distribution, and function of leukocytes (white blood cells) that profoundly influence inflammation and response to infection within the body (In this way, steroids help to mediate the overlap between the endocrine systems [chapter 5] and the immune systems [chapter 6]). Glucocorticoids also suppress inflammation at the molecule level by suppressing inflammatory cytokines, chemokines, and other molecular mediators of inflammation. [Pg.335]

Cytokines chemokines interferons (IFNs) tumor necrosis factor (TNF) interleukins (ILs)... [Pg.190]

Macrophage presence and reactivity in tissue sites are elicited though different combinations of effector molecules (e.g., cytokines, chemokines) acting on specific receptors thus, the expression and presence of given membrane receptors on macrophage cell surfaces correlate to specific (acquired) functions and activation profiles.18 Furthermore, macrophage maturity and/or differentiation state is/are often characterized based on the presence or absence of specific surface receptors (e.g., F4/80 +, Mac-1 + Figure 2.1).61 Receptor profiles vary between cells of different maturity, primary and secondary derivation, and between cell lines.62... [Pg.39]


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See also in sourсe #XX -- [ Pg.52 , Pg.53 , Pg.54 ]




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