AI Article Synopsis
- The innate immune response is a complex system that protects the body from disturbances and pathogens, involving various cell types and humoral components.
- Adipocytokines, a family of proteins, play significant roles in inflammation, with leptin being pro-inflammatory, and adiponectin serving an anti-inflammatory function.
- This review highlights the roles of specific adipokines, such as resistin, visfatin, and chemerin, in modulating the innate immune response and their mixed effects in inflammatory processes.
Article Abstract
The innate immune response is defined as an immensely complex and sophisticated process aimed at defending the organism against any disturbance in the body homeostasis, including invading pathogens. It requires a close cooperation of a vast amount of different cell types, recognized as inflammatory migrating cells, as well as stationary cells that form tissues. Moreover, innate immune mechanisms require an efficient functioning of various humoral components that exert a significant impact on physiological and pathological processes. Apart from commonly mentioned humoral factors, this group also includes a family of proteins known as adipocytokines that may act as pro- or anti-inflammatory agents or act both ways. Leptin, predominantly characterized as a proinflammatory adipokine, plays a crucial role in endothelium remodeling and regulation, as well as in cell survival and production of numerous cytokines. Adiponectin, similar to leptin, acts on the endothelial cells and the phagocytic properties of immune cells; however, it exerts an anti-inflammatory impact. Resistin has a documented role in the control of angiogenesis and stimulation of proinflammatory mediator generation and release. Furthermore, there are adipokines, ie, visfatin and chemerin, whose participation in the inflammatory processes is ambiguous. This review focuses on the current knowledge on the extensive role of selected adipokines in innate immune response.
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| http://dx.doi.org/10.1089/jir.2018.0102 | DOI Listing |
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