Abstract
Leukotriene B4 (LTB4) is one of the major inflammatory mediators responsible for recruiting and activating inflammatory cells. This dihydroxy metabolite of arachidonic acid participates in various leukocyte activities, such as adhesion, chemotaxis, aggregation and degranulation and in the modulation of lymphocyte and mononuclear phagocyte function (1–4). LTB4 also activates PMNs to generate Superoxide anion (5) and release lysosomal enzymes (6). In vivo, intradermal injection of 0.1–100 nmol LTB4 induces neutrophil infiltration, plasma exudation and increased vascular permeability (7). These biological effects have been demonstrated to be mediated by specific G protein-coupled receptors for LTB4 present on neutrophils, eosinophils, lymphocytes and monocytes (2), suggesting that LTB4 may play a role in the development of diseases such as psoriasis, inflammatory bowel diseases, rheumatoid arthritis and chronic asthma by evoking the accumulation and activation of inflammatory cells (8–12). As such, identification of biochemical events in the regulation of receptor integrity may lead to an understanding of the activation of inflammatory cells under pathophysiological conditions.
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Lin, KT., Godfrey, H.P., Spokas, E.G., Sun, F.F., Wong, P.YK. (1999). Modulation of LTB4 Receptor in T-Lymphocytes by Lipoxin A4 (LXA4) and Its Role in Delayed-Type Hypersensitivity. In: Nigam, S., Pace-Asciak, C.R. (eds) Lipoxygenases and their Metabolites. Advances in Experimental Medicine and Biology, vol 447. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4861-4_14
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DOI: https://doi.org/10.1007/978-1-4615-4861-4_14
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