**1. Introduction**

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The inflammatory response is a highly regulated process initiated by tissue damage, infil‐ trating pathogens or both. The primary role of inflammation is the resolution of tissue dam‐ age, including the elimination of damaged or dead cells and any infiltrating pathogens, and restoration of homeostasis. The initial recognition of tissue damage and/or pathogens is mediated by tissue resident macrophages primarily through various sentinel pattern recog‐ nition receptors such as toll-like receptors. In response to and in accordance with distinct stimuli, macrophages become activated to produce a wide range of bioactive molecules, some of which attract other cells to the site of inflammation, and others that dictate the course of an inflammatory response and eventual tissue repair. Recent evidence suggests that there are at least two activation states of monocytes/ macrophages [4, 130, 211, 214]. The classically activated monocytes/macrophages possess significant antimicrobial armamentari‐ um, secrete a plethora of factors that propagate and enhance the microbicidal activities and in general mediate pathogen clearance. The non-classically or alternatively activated mono‐ cytes/macrophages secrete factors that ablate the destructive components of the inflammato‐ ry response and promote tissue healing, repair and angiogenesis and will not be addressed further here.

The processes involved in the onset, progression and resolution of inflammation are com‐ plex and remain to be fully elucidated in vertebrates. However, it is widely believed that myeloid lineage cells are intimately involved in inflammatory reactions and their function is controlled by cytokines. This review focuses on the recent advancements in the understand‐ ing of the biology of hallmark fish pro-inflammatory cytokines, tumor necrosis factor alpha (TNFα), interferon gamma (IFNγ) and interleukin-1 beta (IL-1β) and their receptors.

© 2013 Grayfer and Belosevic; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 Grayfer and Belosevic; licensee InTech. This is a paper distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
