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Proinflammatory cytokines, production

Cho SY, Park SJ, Kwon MJ, Jeong TS, Bok SH, Choi WY, Jeong WI, Ryu SY, Do SH, Lee CS, Song JC and Jeong KS. 2003. Quercetin suppresses proinflammatory cytokines production through MAP kinases andNF-kappaB pathway in lipopolysaccharide-stimulated macrophage. Mol Cell Biochem 243(1-2) 153-160. [Pg.170]

It is possible to identify various factors that confer on chemicals the ability to induce skin sensitization and allergic contact dermatitis. These include the capacity to gain access to the viable epidermis across the stratum corneum, to associate stably with host proteins, to provoke a certain degree of proinflammatory cytokine production by skin cells, and to be recognized by specific T lymphocytes. The effectiveness with which these requirements are met, and possibly other properties of the chemical that influence the vigor of induced immune responses, together with the extent of exposure, will dictate the degree to which sensitization is achieved. [Pg.570]

Histamine actively participates in functions and activity of DC precursors as well as their immature and mature forms. Immature and mature DCs express all four HRs [179-182]. In the differentiation process of type 1 DC from monocytes, HRl and HR3 act as positive stimulants that increase antigen-presentation capacity and proinflammatory cytokine production and Thl-priming activity. In contrast, HR2 acts as a suppressive molecule for antigen-presentation capacity, enhances IL-10 production and induces of IL-lO-producing T cells [183-185]. [Pg.169]

In the case of TSST-1, T-cell activation may be influenced by peptide in the antigen-binding groove of HLA-DR as per contact with the C-terminus ofTSST-1. Specifically, histidines 132, 135, and 140 ofTSST-1 are important for T-cell receptor interactions plus stimulation of proinflammatory cytokine production. This is readily demonstrated by in vitro and in vivo studies with these toxin mutants, which also represent promising... [Pg.162]

F2. Fadok, V. A., Bratton, D. L., Konowal, A., Freed, P. W., Westcott, J. Y., and Henson, P. M., Macrophages that have ingested apoptotic cells in vitro inhibit proinflammatory cytokine production through autocrine/paracrine mechanisms involving TGF-beta, PGE2, and PAF. J. Clin. Invest. 101, 890-898 (1998). [Pg.160]

Kimura A., Sakurada S., Ohkuni H., Todome Y., and Kurata K. (2002) Moderate hypothermia delays proinflammatory cytokine production of human peripheral blood mononuclear cells. Crit. Care Med. 30, 1499-1502. [Pg.143]

Glaser R, Kiecolt-Glaser JK, Maruclia PT, et al. Stress-related changes in proinflammatory cytokine production in wounds. Arch Gen Psychiatry 1999 56 450-6. [Pg.730]

Teunissen MB, Koomen CW, de Waal Malefyt R, Wierenga EA, Bos JD (1998) Interleukin-17 and interferon-gamma synergize in the enhancement of proinflammatory cytokine production by human keratinocytes. J Invest Dermatol 111 645-649 Toumade H, Pelletier L, Pasquier R, Vial MC, Mandet C, Druet P (1990) D-penicillamine-induced autoimmunity in Brown-Norway rats. Similarities with HgC12-induced autoimmunity. J Immunol 144 2985-2991... [Pg.230]

Initial tumor growth, during which the anti-inflammatory activity of lL-10 inhibits reactive cells and their proinflammatory cytokine production, is followed by ELAM-1 expression [55], possibly induced directly by lL-10 in peripheral tumor microvessels [56]. The resulting neutrophil influx and interaction with ECs play a key role in leading to a delayed, but efficacious antitumor reaction with complete tumor eradication. [Pg.187]

At the injury site, PLA2 catalyzed reaction product, arachidonate (ARA), is metabolized to neuroactive pro-inflammatory compounds such as prostaglandin E2 (PGE2), which facilitates macrophage and microglial recruitment at the injury site (see below). In addition, PGE2 also increases local blood flow and leukocyte infiltration and enhances vascular permeability and proinflammatory cytokine production (Amar and Levy, 1999). [Pg.115]

Khan AQ, Nafees S, Sultana S (2011) Perillyl alcohol protects against ethanol induced acute liver injury in Wistar rats by inhibiting oxidative stress, NFk-B activation and proinflammatory cytokine production. Toxicology 279(1-3) 108-114... [Pg.4157]

As to surface proteins, the S-layer protein SlpA of Lact. acidophilus was involved in the modulation of dendritic cells (DCs) and T-cell functions, as it directly interacted with a specific DCs receptor. In fact, the deletion of slpA in mutant strains led to a reduced DCs binding capacity and to an enhanced proinflammatory cytokine production (Konstantinov et al. 2008). Moreova-, tbe amount of SlpA in different Lact. acidophilus strains was related to adhesion to Caco-2 cells as well as to the release of IL-12 from DCs (Ashida et al. 2011). [Pg.164]

Yoshimura, X, Takeda, A., Hamano, S., et al. (2006) Two-sided roles of IL-27 induction of Thl differentiation on naive CD4+ T cells versus suppression of proinflammatory cytokine production including IL-23-induced IL-17 on activated CD4+ T cells partially through STAT3-dependent mechanism. J Immunol 177, 5377-5385. [Pg.189]

Inhibits T-celi proliferation and downregulates proinflammatory cytokine production... [Pg.139]


See other pages where Proinflammatory cytokines, production is mentioned: [Pg.877]    [Pg.644]    [Pg.431]    [Pg.564]    [Pg.74]    [Pg.166]    [Pg.878]    [Pg.212]    [Pg.135]    [Pg.272]    [Pg.84]    [Pg.176]    [Pg.197]    [Pg.281]    [Pg.83]    [Pg.90]    [Pg.1511]    [Pg.18]    [Pg.241]    [Pg.307]    [Pg.1897]    [Pg.2289]    [Pg.31]    [Pg.721]    [Pg.468]   
See also in sourсe #XX -- [ Pg.3058 ]




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Proinflammatory cytokines

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